Chandra Sekhar Bhol
@nus.edu.sg
Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore
National University of Singapore
Dr. Bhol is currently working as a post doctoral fellow in the Department of Pharmacology, National University of Singapore. He has awarded his Ph.D. degree on the topic entitled "Unravelling the molecular connection between PAX9 and autophagy to regulate oral carcinogenesis" from the Department of Life Science, National Institute of Technology Rourkela, India. Prior to it he has done MTech in Agricultural Engineering from IIT Kharagpur and MSc in Life Science from NIT Rourkela.
RESEARCH INTERESTS
Cancer Biology
Scopus Publications
Scholar Citations
Scholar h-index
Scholar i10-index
Scopus Publications
Chandra Sekhar Bhol and Sujit Kumar Bhutia
Elsevier
Chandra Sekhar Bhol, Soumya Ranjan Mishra, Shankargouda Patil, Sunil Kumar Sahu, R Kirtana, Soumen Manna, Muthu Kumaraswamy Shanmugam, Gautam Sethi, Samir Kumar Patra, and Sujit Kumar Bhutia
Elsevier BV
Soumya Ranjan Mishra, Kewal Kumar Mahapatra, Bishnu Prasad Behera, Chandra Sekhar Bhol, Prakash Priyadarshi Praharaj, Debasna Pritimanjari Panigrahi, Srimanta Patra, Amruta Singh, Shankargouda Patil, Rohan Dhiman,et al.
Elsevier BV
Tumour-promoting inflammation is a critical hallmark in cancer development, and inflammasomes are well-known regulators of inflammatory processes within the tumour microenvironment. Different inflammasome components along with the adaptor, apoptosis-associated speck-like protein containing caspase activation and recruitment domain (ASC), and the effector, caspase-1, have a significant influence on tumorigenesis but in a tissue-specific and stage-dependent manner. The downstream products of inflammasome activation, that is the proinflammatory cytokines such as IL-1β and IL-18, regulate tissue homeostasis and induce antitumour immune responses, but in contrast, they can also favour cancer growth and proliferation by directing various oncogenic signalling pathways in cancer cells. Moreover, different epigenetic mechanisms, including DNA methylation, histone modification and noncoding RNAs, control inflammasomes and their components by regulating gene expression during cancer progression. Furthermore, autophagy, a master controller of cellular homeostasis, targets inflammasome-induced carcinogenesis by maintaining cellular homeostasis and removing potential cancer risk factors that promote inflammasome activation in support of tumorigenesis. Here, in this review, we summarize the effect of inflammasome activation in cancers and discuss the role of epigenetic and autophagic regulatory mechanisms in controlling inflammasomes. A proper understanding of the interactions among these key processes will be useful for developing novel therapeutic regimens for targeting inflammasomes in cancer.
Srimanta Patra, Soumya R. Mishra, Bishnu P. Behera, Kewal K. Mahapatra, Debasna P. Panigrahi, Chandra S. Bhol, Prakash P. Praharaj, Gautam Sethi, Samir K. Patra, and Sujit K. Bhutia
Elsevier BV
Autophagy is an intracellular catabolic self-cannibalism that eliminates dysfunctional cytoplasmic cargos by the fusion of cargo-containing autophagosomes with lysosomes to maintain cyto-homeostasis. Autophagy sustains a dynamic interlink between cytoprotective and cytostatic during malignant transformation in a context-dependent manner. The antioxidant and immunomodulatory phyto-products govern autophagy and autophagy-associated signaling pathways to combat cellular incompetence during malignant transformation. Moreover, in a close cellular signaling circuit, autophagy regulates aberrant epigenetic modulation and inflammation, which limits tumor metastasis. Thus, manipulating autophagy for induction of cell death and associated regulatory phenomena will embark on a new strategy for tumor suppression with wide therapeutic implications. Despite the prodigious availability of lead pharmacophores in nature, the central autophagy regulating entities, their explicit target, as well as pre-clinical and clinical assessment remains a major question to be answered. In addition to this, the stage-specific regulation of autophagy and mode of action with natural products in regulating the key autophagic molecules, control of tumor-specific pathways in relation to modulation of autophagic network specify therapeutic target in caner. Moreover, the molecular pathway specificity and enhanced efficacy of the pre-existing chemotherapeutic agents in co-treatment with these phytochemicals hold high prevalence for target specific cancer therapeutics. Hence, the multi-specific role of phytochemicals in a cellular and tumor context dependent manner raises immense curiosity for investigating of novel therapeutic avenues. In this perspective, this review discusses about diverse implicit mechanisms deployed by the bioactive compounds in diagnosis and therapeutics approach during cancer progression with special insight into autophagic regulation.
Prajna Paramita Naik, Swagatika Panigrahi, Ratnakar Parida, Prakash Priyadarshi Praharaj, Chandra Sekhar Bhol, Shankargouda Patil, NML Manjunath, Dipanjan Ghosh, Samir Kumar Patra, and Sujit Kumar Bhutia
Springer Science and Business Media LLC
Cancer stem cells (CSCs) are rare populations of malignant cells with stem cell-like features of self-renewal, uninterrupted differentiation, tumorigenicity, and resistance to conventional therapeutic agents, and these cells have a decisive role in treatment failure and tumor relapse. The self-renewal potential of CSCs with atypical activation of developmental signaling pathways involves the maintenance of stemness to support cancer progression. The acquisition of stemness in CSCs has been accomplished through genetic and epigenetic rewiring following the metabolic switch. In this context, "metabostemness" denotes the metabolic parameters that essentially govern the epitranscriptional gene reprogramming mechanism to dedifferentiate tumor cells into CSCs. Several metabolites often referred to as oncometabolites can directly remodel chromatin structure and thereby influence the operation of epitranscriptional circuits. This integrated metaboloepigenetic dimension of CSCs favors the differentiated cells to move in dedifferentiated macrostates. Some metabolic events might perform as early drivers of epitranscriptional reprogramming; however, subsequent metabolic hits may govern the retention of stemness properties in the tumor mass. Interestingly, selective removal of mitochondria through autophagy can promote metabolic plasticity and alter metabolic states during differentiation and dedifferentiation. In this connection, novel metabostemness-specific drugs can be generated as potential cancer therapeutics to target the metaboloepigenetic circuitry to eliminate CSCs.
Snigdharani Panda, Chandra S. Bhol, Sujit K. Bhutia, and Sasmita Mohapatra
American Chemical Society (ACS)
Chandra Sekhar Bhol, Shankargouda Patil, Binod Bihari Sahu, Samir Kumar Patra, and Sujit Kumar Bhutia
Elsevier BV
Paired box 9 (PAX9) gene belongs to the PAX family, which encodes a family of metazoan transcription factors documented by a conserved DNA binding paired domain 128-amino-acids, critically essential for physiology and development. It is primarily expressed in embryonic tissues, such as the pharyngeal pouch endoderm, somites, neural crest-derived mesenchyme, and distal limb buds. PAX9 plays a vital role in craniofacial development by maintaining the odontogenic potential, mutations, and polymorphisms associated with the risk of tooth agenesis, hypodontia, and crown size in dentition. The loss-of-function of PAX9 in the murine model resulted in a short life span due to the arrest of cleft palate formation and skeletal abnormalities. According to recent studies, the PAX9 gene has a significant role in maintaining squamous cell differentiation, odontoblast differentiation of pluripotent stem cells, deregulation of which is associated with tumor initiation, and malignant transformation. Moreover, PAX9 contributes to promoter hypermethylation and alcohol- induced oro-esophageal squamous cell carcinoma mediated by downregulation of differentiation and apoptosis. Likewise, PAX9 activation is also reported to be associated with drug sensitivity. In summary, this current review aims to understand PAX9 function in the regulation of development, differentiation, and carcinogenesis, along with the underlying signaling pathways for possible cancer therapeutics.
Soumya Ranjan Mishra, Kewal Kumar Mahapatra, Bishnu Prasad Behera, Srimanta Patra, Chandra Sekhar Bhol, Debasna Pritimanjari Panigrahi, Prakash Priyadarshi Praharaj, Amruta Singh, Shankargouda Patil, Rohan Dhiman,et al.
Elsevier BV
The NLR family pyrin domain containing 3 (NLRP3) inflammasome is responsible for the sensation of various pathogenic and non-pathogenic damage signals and has a vital role in neuroinflammation and neural diseases. Various stimuli, such as microbial infection, misfolded protein aggregates, and aberrant deposition of proteins including amyloid-β, α-synuclein can induce NLRP3 inflammasome in neural cells. Once triggered, the NLRP3 inflammasome leads to the activation of caspase-1, which in turn activates inflammatory cytokines, such as interleukin-1β and interleukin -18, and induces pyroptotic cell death. Mitochondria are critically involved in diverse cellular processes and are involved in regulating cellular redox status, calcium levels, inflammasome activation, and cell death. Mitochondrial dysfunction and subsequent accumulation of mitochondrial reactive oxygen species, mitochondrial deoxyribonucleic acid, and other mitochondria-associated proteins and lipids play vital roles in the instigation of the NLRP3 inflammasome. In addition, the processes of mitochondrial dynamics, such as fission and fusion, are essential in the maintenance of mitochondrial integrity and their imbalance also promotes NLRP3 inflammasome activation. In this connection, mitophagy-mediated maintenance of mitochondrial homeostasis restricts NLRP3 inflammasome hyperactivation and its consequences in various neurological disorders. Hence, mitophagy can be exploited as a potential strategy to target damaged mitochondria-derived NLRP3 inflammasome activation and its lethal consequences. Therefore, the identification of novel mitophagy modulators has promising therapeutic potential for NLRP3 inflammasome-associated neuronal diseases.
Snigdharani Panda, Chandra Sekhar Bhol, Sujit Kumar Bhutia, and Sasmita Mohapatra
Royal Society of Chemistry (RSC)
A hybrid nanoparticle consisting of N-doped mesoporous carbon nanospheres as core and thermosensitive PEG–PEI as outer shell shows multiple therapeutic actions such as PTT, PDT and NIR sensitive drug release under single 980 nm laser excitation.
Srimanta Patra, Kewal Kumar Mahapatra, Prakash Priyadarshi Praharaj, Debasna Pritimanjari Panigrahi, Chandra Sekhar Bhol, Soumya Ranjan Mishra, Bishnu Prasad Behera, Amruta Singh, Mrutyunjay Jena, and Sujit Kumar Bhutia
Elsevier BV
Mitochondrial quality control is crucial for sustaining cellular maintenance. Mitochondrial Ca2+ play an important role in the maintenance of mitochondrial quality control through regulation of mitochondrial dynamics, mitophagy and mitochondrial biogenesis for preserving cellular homeostasis. The regulation of this dynamic interlink between these mitochondrial networks and mitochondrial Ca2+ appears indispensable for the adaptation of cells under external stimuli. Moreover, dysregulation of mitochondrial Ca2+ divulges impaired mitochondrial control that results in several pathological conditions such as cancer. Hence this review untangles the interplay between mitochondrial Ca2+ and quality control that govern mitochondrial health and mitochondrial coordinates in the development of cancer.
Debasna P. Panigrahi, Chandra S. Bhol, R. Nivetha, Siddavaram Nagini, Shankargouda Patil, Tapas K. Maiti, and Sujit K. Bhutia
Elsevier BV
Prakash Priyadarshi Praharaj, Debasna Pritimanjari Panigrahi, Chandra Sekhar Bhol, Srimanta Patra, Soumya Ranjan Mishra, Kewal Kumar Mahapatra, Bishnu Prasad Behera, Amruta Singh, Shankargouda Patil, and Sujit Kumar Bhutia
Elsevier BV
Cancer stem cells (CSCs) are distinct subpopulations of cancer cells with stem cell-like abilities and are more resilient to chemotherapy, causing tumor relapse. Mitophagy, a selective form of autophagy, removes damaged unwanted mitochondria from cells through a lysosome-based degradation pathway to maintain cellular homeostasis. CSCs use mitophagy as a chief survival response mechanism for their growth, propagation, and tumorigenic ability. Mitochondrial biogenesis is a crucial cellular event replacing damaged mitochondria through the coordinated regulation of several transcription factors to achieve the bioenergetic demands of the cell. Because of the high mitochondrial content in CSCs, mitochondrial biogenesis is an interesting target to address the resistance mechanisms of anti-CSC therapy. However, to what extent both mitophagy and mitochondrial biogenesis are vital in promoting stemness, metabolic reprogramming, and drug resistance in CSCs has yet to be established. Therefore, in this review, we focus on understanding the interesting aspects of mitochondrial rewiring that involve mitophagy and mitochondrial biogenesis in CSCs. We also discuss their coordinated regulation in the elimination of CSCs, with respect to stemness and differentiation of the CSC phenotype, and the different aspects of tumorigenesis such as cancer initiation, progression, resistance, and tumor relapse. Finally, we address several other unanswered questions relating to targeted anti-CSC cancer therapy, which improves patient survival.
Prajna Paramita Naik, Subhadip Mukhopadhyay, Prakash Priyadarshi Praharaj, Chandra Sekhar Bhol, Debasna Pritimanjari Panigrahi, Kewal Kumar Mahapatra, Srimanta Patra, Sarbari Saha, Aditya Kumar Panda, Krupasindhu Panda,et al.
Elsevier BV
AIMS
Secretory clusterin (sCLU) plays an important role in tumor development and cancer progression. However, the molecular mechanisms and physiological functions of sCLU in oral cancer is unclear. We examined the impact of sCLU-mediated autophagy in cell survival and apoptosis inhibition in oral cancer.
MAIN METHODS
Immunohistochemical analysis was performed to analyze protein expression in patient samples. Autophagy and mitophagy was studied by immunofluorescence microscopy and Western blot. The gain and loss of function was studied by overexpression of plasmid and siRNA approaches. Cellular protection against nutrient starvation and therapeutic stress by sCLU was studied by cell viability assay and caspase assay.
KEY FINDINGS
The data from oral cancer patients showed that the expression levels of sCLU, ATG14, ULK1, and PARKIN were increase grade wise manners. Interestingly, sCLU overexpression promoted autophagy through AMPK/Akt/mTOR signaling pathway leading to cell survival and protection from long exposure serum starvation induced-apoptosis. Additionally, sCLU was demonstrated to interact with ULK1 and inhibition ULK1 activity by SBI206965 was found to abolish sCLU-induced autophagy indicating critical role of ULK1 in induction of autophagy. Furthermore, sCLU was observed to promote expression of mitophagy-associated proteins in serum starvation conditions to protect OSCC cells from nutrient deprivation. The meta-analysis elucidated that high CLU expression is associated with therapy resistance in cancer and we demonstrated that sCLU-mediated mitophagy was revealed to inhibit OSCC cell death by cisplatin.
SIGNIFICANCE
The present investigation has highlighted the probable implications of the clusterin-induced autophagy in cell survival and inhibition of apoptosis in oral cancer.
Srimanta Patra, Chandra Sekhar Bhol, Debasna Pritimanjari Panigrahi, Prakash Priyadarshi Praharaj, Biswajita Pradhan, Mrutyunjay Jena, and Sujit Kumar Bhutia
Elsevier BV
Ionizing radiation has the potential to cause structural modification or change in electrochemical properties in parent lead pharmacophores that exhibit enhanced bioactivity. Gallic acid (GA), a triphenolic compound has displayed potent anticancer drug potency due to its withstanding antioxidant propensity. This study uncovered the comparative efficacy of gamma-irradiated gallic acid (GAIR) in the modulation of an antioxidant system for regulation apoptosis and autophagy. GAIR exhibited remarkable anti-proliferative efficacy as shown by MTT, clonogenic survival, and scratch assay. In addition to this, GAIR promoted intrinsic apoptosis through mitochondrial reactive oxygen species (ROS) i.e. mitochondrial superoxide generation. GAIR decreased the activity of antioxidant enzymes by downregulating nuclear factor erythroid 2-related factor 2 (NRF2) and downstream effector molecules NAD(P)H Quinone Dehydrogenase 1 (NQO1) and gamma-glutamylcysteine synthetase (GCLC). Simultaneously, GAIR attenuated autophagosome-lysosome fusion without altering the lysosomal activity. Inhibition of autophagic flux resulted in the accumulation of lipid droplets (LDs) such as hexadecanoic acid and oleic acid that fueled ROS generation leading to apoptosis. In the meantime, under oxidative upset, conversion of LDs to free fatty acids reduced leading to inhibition of ATP generation that subsequently provoked apoptosis. The investigation of the effects of autophagy inhibition by GAIR on the therapeutic efficacy of chemotherapeutic drugs was done and the co-treatment markedly decreased the cell viability and increased apoptosis. Further, the in vivo efficacy of the drug was investigated in Dalton's Lymphoma-tumor bearing mice. The modulation of apoptosis and autophagy in tumor inhibition was determined. In conclusion, the study proposed, change in electrochemical properties by gamma radiation enhances the anticancer efficacy of gallic acid through ROS mediated apoptosis fuelled by inhibition of lipophagy in an NRF2 dependent signaling pathway.
Debasna P. Panigrahi, Prakash P. Praharaj, Chandra S. Bhol, Kewal K. Mahapatra, Srimanta Patra, Bishnu P. Behera, Soumya R. Mishra, and Sujit K. Bhutia
Elsevier BV
Mitophagy is an evolutionarily conserved cellular process which selectively eliminates dysfunctional mitochondria by targeting them to the autophagosome for degradation. Dysregulated mitophagy results in the accumulation of damaged mitochondria, which plays an important role in carcinogenesis and tumor progression. The role of mitophagy receptors and adaptors including PINK1, Parkin, BNIP3, BNIP3L/NIX, and p62/SQSTM1, and the signaling pathways that govern mitophagy are impaired in cancer. Furthermore, the contribution of mitophagy in regulating the metabolic switch may establish a balance between aerobic glycolysis and oxidative phosphorylation for cancer cell survival. Moreover, ROS-driven mitophagy achieves different goals depending on the stage of tumorigenesis. Mitophagy promotes plasticity in the cancer stem cell through the metabolic reconfiguration for better adaption to the tumor microenvironment. In addition, the present review sheds some light on the role of mitophagy in stemness and differentiation during the transition of cell's fate, which could have a crucial role in cancer progression and metastasis. In conclusion, this review deals with the detailed molecular mechanisms underlying mitophagy, along with highlighting the dual role of mitophagy in different aspects of cancer, suggesting it as a possible target in the mitophagy-modulated cancer therapy.
Chandra S. Bhol, Debasna P. Panigrahi, Prakash P. Praharaj, Kewal K. Mahapatra, Srimanta Patra, Soumya R. Mishra, Bishnu P. Behera, and Sujit K. Bhutia
Elsevier BV
Epigenetic alterations, such as DNA methylation, histone modifications and miRNAs, have a significant role play in malignant cellular transformation and metastasis. On the other hand, autophagy has been reported to perform context-dependent roles in cancer; at times, it becomes lethal and abolishes tumorigenesis, whereas, at other instances, it protects cancer cells by providing a rescue mechanism under adverse conditions. Although epigenetics and autophagy are two important and independent cellular processes, various oncogenic and oncosuppressor proteins involve autophagy through epigenetic modifications and different signaling pathways, thereby regulating tumor growth and therapeutic response. Moreover, the importance of epigenetic modification of autophagy in cancer is reflected through its involvement in cancer stem cell maintenance, which in turn, contributes to tumor cell viability during dormancy leading to tumor recurrence. The effects of epigenetic modifications of autophagy in cancer is still ambiguous and less acknowledged; therefore, efforts have been made to understand its detail underlying mechanism to unveil new targets and avenues for better prognosis and diagnosis of cancer.
Srimanta Patra, Prakash Priyadarshi Praharaj, Debasna Pritimanjari Panigrahi, Biswajit Panda, Chandra Sekhar Bhol, Kewal Kumar Mahapatra, Soumya Ranjan Mishra, Bishnu Prasad Behera, Mrutyunjay Jena, Gautam Sethi,et al.
Springer Science and Business Media LLC
Marine invertebrates are extremely diverse, largely productive, untapped oceanic resources with chemically unique bioactive lead compound contributing a wide range of screening for the discovery of anticancer compounds. The lead compounds have unfurled an extensive array of pharmacological properties owing to the presence of polyphenols, alkaloids, terpenoids and other secondary metabolites. The antioxidant, immunomodulatory and anti-tumor activities exhibited, are possibly regulated by the apoptosis induction, scavenging of ROS and modulation of cellular signaling pathways to defy the cellular deafness during carcinogenesis. Despite the enriched bioactive compounds, the marine invertebrates are largely unexplored as identification, screening, pre-clinical and clinical assessment of lead compounds and their synthetic analogs remain a major task to be solved. In the current review, we focus on the principle strategy and underlying mechanisms deployed by the bioactive anticancer compounds derived from marine invertebrates to combat cancer with special insight into the cell death mechanism.
Debasna P. Panigrahi, Chandra S. Bhol, Nivetha R, Siddavaram Nagini, Shankargouda Patil, Tapas K. Maiti, and Sujit K. Bhutia
Elsevier BV
Abrus agglutinin (AGG), a heterotetrameric type II ribosome inactivating protein isolated from the seeds of Abrus precatorius shows potent antitumor activity in different cancer models. We examined the role of antioxidant system in modulation of the anticancer activity of AGG in in vitro and in hamster model of oral cancer. AGG promotes apoptosis through accumulation of ROS in CAL33 cells. Interestingly, our data showed that AGG decreases the activity of antioxidant enzymes including superoxide dismutase, catalase, glutathione peroxidase in CAL33 cells indicating antioxidant enzyme inhibition leads to AGG-induced ROS accumulation. Moreover, AGG inhibits expression of NRF2, transcription factor which regulates the expression of antioxidant enzymes in CAL33 cells. We found that AGG induces autophagy induction and loss of p62 expression in CAL33 cells. Furthermore, it showed that NRF2 expression is restored in the presence of 3-methyladenine and Baficomycin-A1 establishing role of autophagy in modulation of NRF2 through p62. Our study showed that AGG significantly inhibited tumor growth in DMBA-induced carcinogenesis. In immunohistochemical analysis, AGG-treated tumor displays higher caspase3 expression and less p62 and NRF2 expression in comparison to the control. In conclusion, AGG-induced degradation of NRF2 through autophagy leads to ROS accumulation dependent apoptosis which might be used for treatment of oral cancer.
Srimanta Patra, Prashanta Kumar Panda, Prajna Paramita Naik, Debasna Pritimanjari Panigrahi, Prakash Priyadarshi Praharaj, Chandra Sekhar Bhol, Kewal Kumar Mahapatra, Priyadarshini Padhi, Mrutyunjay Jena, Shankargouda Patil,et al.
Elsevier BV
Terminalia bellirica (TB) has been used in traditional Indian medical system, Ayurveda. However, the mechanism underlying the efficacy of the TB extract against oral squamous cell carcinoma (OSCC) is yet to be explored. The present study established a connecting link between the TB extract induced apoptosis and autophagy in relation to reactive oxygen species (ROS). Our study revealed that gallic acid in the TB extract possess a strong free radical scavenging capacity contributing towards selective anti-proliferative activity. Furthermore, TB extract markedly enhanced the accumulation of ROS that facilitated mitochondrial apoptosis through DNA damage, indicating ROS as the vital component regulating apoptosis. This effect was effectively reversed by the use of a scavenger, N-acetyl cysteine (NAC). Moreover, it was observed to induce autophagy; however, it attenuated the autophagosome-lysosome fusion in Cal33 cells without altering the lysosomal activity. Pharmacological inhibitors of autophagy, namely, 3-methyladenine and chloroquine, were observed to regulate the stage-specific progression of autophagy post treatment with the TB extract, favouring subsequent activation of apoptosis. These findings revealed presence of gallic acid in TB extract below NOAEL value causes oxidative upset in oral cancer cells and promote programmed cell death which has a potential therapeutic value against oral squamous cell carcinoma.
Vanishri Chandrashekhar Haragannavar, Roopa S. Rao, Kewal Kumar Mahapatra, Srimanta Patra, Bishnu Prasad Behera, Amruta Singh, Soumya Ranjan Mishra, Chandra Sekhar Bhol, Debasna Pritimanjari Panigrahi, Prakash Priyadarshi Praharaj,et al.
Springer Singapore
Prakash Priyadarshi Praharaj, Bishnu Prasad Behera, Soumya Ranjan Mishra, Srimanta Patra, Kewal Kumar Mahapatra, Debasna Pritimanjari Panigrahi, Chandra Sekhar Bhol, and Sujit Kumar Bhutia
Springer Singapore
Kewal Kumar Mahapatra, Soumya Ranjan Mishra, Bishnu Prasad Behera, Prakash Priyadarshi Praharaj, Debasna Pritimanjari Panigrahi, Chandra Sekhar Bhol, Srimanta Patra, and Sujit Kumar Bhutia
Springer Singapore
Rahul. K. Das, Snigdharani Panda, Chandra Sekhar Bhol, Sujit. K. Bhutia, and Sasmita Mohapatra
American Chemical Society (ACS)
Use of nanomaterials blessed with both therapeutic and diagnostic property is a proficient strategy in the treatment of cancer in its early stage. In this context, our paper reports the synthesis of uniform size N-rich mesoporous carbon nanospheres of size 65-70 nm from pyrrole and aniline precursor using triton-X as a structure directing agent. TEM microscopy reveals that these carbons spheres contain void spaces in which ultra-small nitrogen doped quantum dots (NCQD) are captured with in the matrix. These mesoporous hollow NCQD captured carbon spheres (NCQD-HCS) show fluorescence quantum yield up to 14.6% under λex=340 nm. Interestingly, samples calcined at >800 ˚C clearly absorb in the wavelength range 700-1000 nm and shows light-to-heat conversion efficiency up to 52%. In vitro experiments in human oral cancer cells (FaDu) show that NCQD-HCS are internalized by the cells and induce substantial thermal ablation effect in FaDu cells when exposed under 980 nm NIR laser.
Srimanta Patra, Debasna P. Panigrahi, Prakash P. Praharaj, Chandra S. Bhol, Kewal K. Mahapatra, Soumya R. Mishra, Bishnu P. Behera, Mrutyunjay Jena, and Sujit K. Bhutia
Springer Science and Business Media LLC
Dysregulation of the epigenome and constitutional epimutation lead to aberrant expression of the genes, which regulate cancer initiation and progression. Histone deacetylases (HDACs), which are highly conserved in yeast to humans, are known to regulate numerous proteins involved in the transcriptional regulation of chromatin structures, apoptosis, autophagy, and mitophagy. In addition, a non-permissive chromatin conformation is created by HDACs, preventing the transcription of the genes encoding the proteins associated with tumorigenesis. Recently, an expanding perspective has been reported from the clinical trials with HDACis (HDAC inhibitors), which has emerged as a determining target for the study of the detailed mechanisms underlying cancer progression. Therefore, the present review focuses on the comprehensive lucubration of post-translational modifications and the molecular mechanisms through which HDACs alter the ambiguities associated with epigenome, with particular insights into the initiation, progression, and regulation of cancer.
Prashanta Kumar Panda, Subhadip Mukhopadhyay, Berendra Behera, Chandra Sekhar Bhol, Sandeep Dey, Durgesh Nandini Das, Niharika Sinha, Akalabya Bissoyi, Krishna Pramanik, Tapas K. Maiti,et al.
Elsevier BV