Dr. Santosh Kumar is an Associate Professor of Biotechnology at Guru Ghasidas Vishwavidyalaya, India, and a cancer biologist with over a decade of international research experience spanning premier institutions in India and the United States. His research program focuses on uncovering fundamental mechanisms of cancer progression, with particular emphasis on mitochondrial biology, metabolic reprogramming, therapy resistance, and cancer stem cell dynamics.
Dr. Kumar obtained his Ph.D. from the National Centre for Cell Science (NCCS), Pune, and subsequently trained at globally renowned institutions including MD Anderson Cancer Center, Baylor College of Medicine, University of Houston, and the University of Mississippi Medical Center. His work across these institutions has provided critical insights into oncogenic signaling, mitochondrial–nuclear crosstalk, SUMOylation, and inflammation-driven tumor progression.
As a recipient of the prestigious DST Ramanujan Fellowship, Dr. Kumar establ
EDUCATION
Ph.D. Biotechnology, National centre for cell science, Pune, 2009
RESEARCH, TEACHING, or OTHER INTERESTS
Cancer Research, Biotechnology, Molecular Biology, Endocrinology
24
Scopus Publications
1727
Scholar Citations
21
Scholar h-index
22
Scholar i10-index
Scopus Publications
Green Tea's EGCG: Brewing Hope in the Battle against Breast Cancer Manoj Kumar, Roop Lal, Amit Sehgal, Suman Rawat, Ankit Kumar, Santosh Kumar, Sunil Kumar Dhatwalia Natural Products Journal, 2026 Breast cancer, a pervasive global malignancy, is anticipated to undergo a significant increase by 2040. Despite the conventional armamentarium of treatments including chemotherapy, radiation therapy, and surgery, the intricate landscape of breast cancer, characterized by its multifaceted surface receptors and signalling pathways, presents formidable challenges to treatment efficacy. Epigallocatechin-3-gallate (EGCG), extracted from Camellia sinensis, has emerged as a subject of interest due to its robust antioxidative properties stemming from its chemical structure. EGCG exerts its effects on pivotal stages of tumour growth and proliferation by modulating key signalling pathways such as MAPK, PI3K, NFkB, and ERK1/2 influencing apoptosis and cell cycle regulation. Clinical trials have provided insights into EGCG's potential impact on breast cancer such as mammographic density and pharmacokinetics, indicating its potential as a potent therapeutic agent. Moreover, when administered with conventional chemotherapy, EGCG demonstrates synergistic effects, enhancing therapeutic outcomes. Nevertheless, further research is warranted to validate the safety and efficacy of EGCG in breast cancer prevention and treatment.
Introduction to microbiomes in health and diseases Prachi Agrawal, Prachi Mendhey, Robins Kumar, Subham Patel, Prakash Kumar Kaushik, Abhishek Dadsena, Santosh Kumar International Review of Cell and Molecular Biology, 2025
Imidazo[1,2-a]Quinoxaline-2-Carbonitrile Derivative (RA-22) Inhibits Self-Renewal and Growth of Cancer Stem and Cancer Cells via Downregulating AKT Pathway Pramit Kumar, Umesh Prasad Yadav, Gaurav Joshi, Sahil Arora, Manvendra Kumar, Joydeep Chatterjee, Vikas Chandra, Sandeep Singh, Raj Kumar, Santosh Kumar Chemistryselect, 2024 EGFR activation in colorectal and breast cancer stimulates downstream pathways like Ras/Raf/MEK/ERK and PI3 K/Akt, fostering cell proliferation, invasion, metastasis, and therapy resistance, underscoring its significance as a therapeutic target in both cancers. In the present work, we rationally designed ( E )‐4‐methyl‐1‐((3‐oxo‐1‐phenylbutyl)amino)‐4‐styryl‐4,5‐dihydroimidazo[1,2‐a]quinoxaline‐2‐carbonitrile ( RA‐22 ) as EGFR inhibitor. Our research investigates the role of RA‐22 as a target molecule for EGFR, exploring its anticancer potential and mechanism of action across breast cancer and colorectal cancer cell lines. The in‐vitro studies showed its cytotoxic response towards MDA‐MB‐231 and HCT‐116 and its inhibitory effect on cancer stem cells in mammosphere/spheroid culture. The compound downregulates the oncogenic signalling proteins like STAT‐3, AKT, PAN‐AKT, and ERK and also reduces the expression of the anti‐apoptotic protein Bcl‐2 and increases the apoptotic proteins like Cleaved‐PARP, Cleaved‐Caspase‐3, and Cleaved‐Caspase‐9.
Natural Compound-Based Nanoparticles to Target Free Radicals in Cancer Umesh Prasad Yadav, M. Rhuthuparna, Kanika Vasudeva, Prabhat Suman, Anjana Munshi, Santosh Kumar, Sandeep Singh Handbook of Oxidative Stress in Cancer Therapeutic Aspects Volume 1, 2022 Cell proliferation and malignant transformation are enabled by genetic and epigenetic changes. During the malignancy process, malignant cells acquire distinguishing characteristics. Cancer cells have acquired the ability to generate more reactive oxygen species (ROS), resulting in high oxidative stress. ROS-mediated signaling is needed for cancer cell physiology, and high levels of ROS cause oxidative stress-induced cytotoxicity in cancer cells. To avoid ROS-mediated cytotoxicity, cancer cells modulate their redox state through various antioxidant mechanisms and keep their ROS levels below the threshold. Cancer treatment that targets oxidative stress is an appealing option. Many natural oxidative stress modulators and bioactive compounds have been used in the treatment of cancer. Conventional uptake of bioactive molecule is associated with lower bioavailability, solubility, unlikely biodistribution, and side effects. Traditional drug uptake is improved by nanoformulation, making it easier to overcome side effects, improve biodistribution, and extend drug duration time. Natural prooxidant-loaded nanoparticles efficiently carry prooxidant to the tumor site and selectively and efficiently induce oxidative stress-mediated cell death in cancer cells.
Let-7a induces metabolic reprogramming in breast cancer cells via targeting mitochondrial encoded ND4 Praveen Sharma, Vibhuti Sharma, Tarunveer Singh Ahluwalia, Nilambra Dogra, Santosh Kumar, Sandeep Singh Cancer Cell International, 2021 Background and objectives MicroRNA (miRNA) that translocate from the nucleus to mitochondria are referred to as mitochondrial microRNA (mitomiR). Albeit mitomiRs have been shown to modulate gene expression, their functional impact within mitochondria is unknown. The main objective of this study is to investigate whether the mitochondrial genome is regulated by miR present inside the mitochondria. Methods and results Here, we report mitomiR let-7a regulates mitochondrial transcription in breast cancer cells and reprogram the metabolism accordingly. These effects were mediated through the interaction of let-7a with mtDNA, as studied by RNA pull-down assays, altering the activity of Complex I in a cell line-specific manner. Our study, for the first time, identifies the role of mitomiR (let-7a) in regulating the mitochondrial genome by transcriptional repression and its contribution to regulating mitochondrial metabolism of breast cancer cells. Conclusion These findings uncover a novel mechanism by which mitomiR regulates mitochondrial transcription.
Metabolic Adaptations in Cancer Stem Cells Umesh Prasad Yadav, Tashvinder Singh, Pramit Kumar, Praveen Sharma, Harsimrat Kaur, Sadhana Sharma, Sandeep Singh, Santosh Kumar, Kapil Mehta Frontiers in Oncology, 2020 Cancer stem cells (CSCs) are a small and elusive subpopulation of self-renewing cancer cells with remarkable ability to initiate, propagate, and spread the malignant disease. In addition, they exhibit increased resistance to anticancer therapies, thereby contributing to disease relapse. CSCs are reported to be present in many tumor types such as melanoma, sarcoma, mammary tumors, colon cancer and other solid tumors. These cells from different tumors show unique energetic and metabolic pathways. For example, CSCs from one type of tumor may predominantly use aerobic glycolysis, while from another tumor type may utilize oxidative phosphorylation. Most commonly these cells use fatty acid oxidation and ketone bodies as the main source of energy production. CSCs have a remarkable ability to reprogram their metabolism in order to survive under adverse conditions such as hypoxia, acidosis, and starvation. There is increasing interest to identify molecular targets that can be utilized to kill CSCs and to control their growth. In this review, we discuss how an understanding of the unique metabolism of CSCs from different tumors can offer promising strategies for targeting CSCs and hence to prevent disease relapse and to treat the metastatic disease.
CAR T cell therapy: newer approaches to counter resistance and cost Rajesh Kumar Yadav, Asgar Ali, Santosh Kumar, Alpana Sharma, Basab Baghchi, Pritanjali Singh, Sushmita Das, Chandramani Singh, Sadhana Sharma Heliyon, 2020 The genetically engineered Chimeric Antigen Receptor bearing T-cell (CAR T cell) therapy has been emerged as the new paradigm of cancer immunotherapy. However, recent studies have reported an increase in the number of relapsed haematological malignancies. This review provides newer insights into how the efficacy of CAR T cells might be increased by the application of new genome editing technologies, monitoring the complexity of tumor types and T cells sub-types. Next, tumor mutation burden along with tumormicroenvironment and epigenetic mechanisms of CAR T cell as well as tumor cell may play a vital role to tackle the cancer resistance mechanisms. These studies highlight the need to consider traditional cancer therapy in conjunction with CAR T cell therapy for relapsed or cases unresponsive to treatment. Of note, this therapy is highly expensive and requires multi-skill for successful implementation, which results in reduction of its accessibility/affordability to the patients. Here, we also propose a model for cost minimization of CAR T cell therapy by a collaboration of academia, hospitals and industry.
Fatty Acid Oxidation-Driven Src Links Mitochondrial Energy Reprogramming and Oncogenic Properties in Triple-Negative Breast Cancer Jun Hyoung Park, Sajna Vithayathil, Santosh Kumar, Pi-Lin Sung, Lacey Elizabeth Dobrolecki, Vasanta Putluri, Vadiraja B. Bhat, Salil Kumar Bhowmik, Vineet Gupta, Kavisha Arora, Danli Wu, Efrosini Tsouko, Yiqun Zhang, Suman Maity, Taraka R. Donti, Brett H. Graham, Daniel E. Frigo, Cristian Coarfa, Patricia Yotnda, Nagireddy Putluri, Arun Sreekumar, Michael T. Lewis, Chad J. Creighton, Lee-Jun C. Wong, Benny Abraham Kaipparettu Cell Reports, 2016
Intercellular Mitochondrial Trafficking as a Master Regulator of Tumor Progression and Cancer Stem Cell Plasticity P Agrawal, S Tiwari, P Mendhey, P Jampala, H Rajak, N Kurrey, N Ahmed, ... Onco 6 (2) , 2026 2026
Antioxidants ameliorates glucose/glucose oxidase-induced myocardial damage through mitochondrial and MAPK pathway S Kumar, P Agrawal, P Mendhey, SK Dhatwalia, SL Sitasawad 3 Biotech 15 (9), 323 , 2025 2025
Green Tea's EGCG: Brewing Hope in the Battle against Breast Cancer M Kumar, R Lal, A Sehgal, S Rawat, A Kumar, S Kumar, SK Dhatwalia The Natural Products Journal , 2025 2025 Citations: 1
Introduction to microbiomes in health and diseases P Agrawal, P Mendhey, R Kumar, S Patel, PK Kaushik, A Dadsena, ... International Review of Cell and Molecular Biology 394, 1-42 , 2025 2025 Citations: 3
Synthesis, Characterization, and Comparative Analysis of Zinc Oxide Nanoparticles using Calendula Officinalis Flower Extract and its Antibacterial Activity L Radhakrishnan, SA Sathar, S Jamal, S Kumar, N Ahmed 2025 Citations: 1
Imidazo[1,2‐ a ]Quinoxaline‐2‐Carbonitrile Derivative (RA‐22) Inhibits Self‐Renewal and Growth of Cancer Stem and Cancer Cells via Downregulating AKT Pathway P Kumar, U Prasad Yadav, G Joshi, S Arora, M Kumar, J Chatterjee, ... ChemistrySelect 9 (23), e202400223 , 2024 2024 Citations: 3
Natural compound-based nanoparticles to target free radicals in cancer UP Yadav, M Rhuthuparna, K Vasudev, P Suman, A Munshi, S Kumar, ... Handbook of Oxidative Stress in Cancer: Therapeutic Aspects, 1-14 , 2022 2022 Citations: 2
Handbook of Oxidative Stress in Cancer: Therapeutic Aspects. Book Chapter-Natural Compound-Based Nanoparticles to Target Free Radicals in Cancer. SS Yadav UP, Rhuthuparna M, Vasudev K, Suman P, Munshi A, Santosh Kumar 2022
Design, synthesis and anticancer activity of 2-arylimidazo [1, 2-a] pyridinyl-3-amines UP Yadav, AJ Ansari, S Arora, G Joshi, T Singh, H Kaur, N Dogra, ... Bioorganic Chemistry 118, 105464 , 2022 2022 Citations: 26
Let-7a induces metabolic reprogramming in breast cancer cells via targeting mitochondrial encoded ND4 P Sharma, V Sharma, TS Ahluwalia, N Dogra, S Kumar, S Singh Cancer cell international 21 (1), 629 , 2021 2021 Citations: 29
Metabolic adaptations in cancer stem cells UP Yadav, T Singh, P Kumar, P Sharma, H Kaur, S Sharma, S Singh, ... Frontiers in oncology 10, 1010 , 2020 2020 Citations: 151
CAR T cell therapy: newer approaches to counter resistance and cost RK Yadav, A Ali, S Kumar, A Sharma, B Baghchi, P Singh, S Das, C Singh, ... Heliyon 6 (4) , 2020 2020 Citations: 34
E-pharmacophore guided discovery of pyrazolo [1, 5-c] quinazolines as dual inhibitors of topoisomerase-I and histone deacetylase G Joshi, S Kalra, UP Yadav, P Sharma, PK Singh, S Amrutkar, AJ Ansari, ... Bioorganic Chemistry 94, 103409 , 2020 2020 Citations: 41
Twist1 Activation in Muscle Progenitor Cells Causes Muscle Loss Akin to Cancer Cachexia AA Santosh Kumar, Parash Parajuli, Audrey Loumaye, Purba Singh, Sailaja ... Developmental Cell 45, 712–725 , 2018 2018 Citations: 63
Abstract A38: Twist1-driven fatty pancreas formation facilitates pancreatitis and pancreatic ductal adenocarcinoma progression TL Nguyen, P Singh, P Parajuli, L Li, C Prunier, S Kumar, S Eragmerdi, ... Cancer Research 78 (10_Supplement), A38-A38 , 2018 2018
Twist1 activation in muscle progenitor cells during development or adulthood causes severe muscle loss reminiscent of human cancer cachexia. P Parajuli, S Kumar, A Loumaye, P Singh, S Eragamreddy, TL Nguyen, ... CANCER RESEARCH 78 (10), 49-50 , 2018 2018
Twist1-driven fatty pancreas formation facilitates pancreatitis and pancreatic ductal adenocarcinoma progression. TL Nguyen, P Singh, P Parajuli, L Li, C Prunier, S Kumar, S Eragmerdi, ... CANCER RESEARCH 78 (10), 49-49 , 2018 2018
Abstract A40: Twist1 activation in muscle progenitor cells during development or adulthood causes severe muscle loss reminiscent of human cancer cachexia AA Parash Parajuli, Santosh Kumar, Audrey Loumaye, Purba Singh, Sailaja ... Cancer Research 78 (10), A40 , 2018 2018
Abstract A38: Twist1-driven fatty pancreas formation facilitates pancreatitis and pancreatic ductal adenocarcinoma progression AA Thien Ly Nguyen, Purba Singh, Parash Parajuli, Lianna Li, Celine Prunier ... Cancer research 10 (78), A38 , 2018 2018
Abstract B33: Tgif inactivation defines a synthetic lethal interaction among oncogenic Kras and Twist1 in pancreatic ductal adenocarcinoma P Parajuli, P Singh, Z Wang, S Kumar, L Li, S Eragamreddi, TL Nguyen, ... Molecular Cancer Therapeutics 16 (10_Supplement), B33-B33 , 2017 2017
MOST CITED SCHOLAR PUBLICATIONS
Fatty acid oxidation-driven Src links mitochondrial energy reprogramming and oncogenic properties in triple-negative breast cancer JH Park, S Vithayathil, S Kumar, PL Sung, LE Dobrolecki, V Putluri, ... Cell reports 14 (9), 2154-2165 , 2016 2016 Citations: 359
Metabolic adaptations in cancer stem cells UP Yadav, T Singh, P Kumar, P Sharma, H Kaur, S Sharma, S Singh, ... Frontiers in oncology 10, 1010 , 2020 2020 Citations: 151
Tissue transglutaminase constitutively activates HIF-1α promoter and nuclear factor-κB via a non-canonical pathway S Kumar, K Mehta Plos One 7 (11), e49321 , 2012 2012 Citations: 137
Tissue transglutaminase as a central mediator in inflammation-induced progression of breast cancer N Agnihotri, S Kumar, K Mehta Breast Cancer Research 15 (1), 202 , 2013 2013 Citations: 128
N-Acetyl Cysteine prevents glucose/glucose oxidase-induced oxidative stress, mitochondrial damage and apoptosis in H9c2 cells. SKSL Sitasawad Life Science 84 (11-12), 328-336 , 2009 2009 Citations: 123
Multiple antioxidants improve cardiac complications and inhibit cardiac cell death in streptozotocin-induced diabetic rats SPSLS Santosh Kumar PLoS One 8 (7), e67009 , 2013 2013 Citations: 90
Cadmium induced mitochondrial injury and apoptosis in Vero cells: Protective effect of diallyl tetrasulfide from garlic. KS Murugavel P, Pari L, Sitasawad SL, Kumar S Int J Biochem Cell Biol. 39 (1), 161-170 , 2007 2007 Citations: 90
Evidence that GTP-binding domain but not catalytic domain of transglutaminase 2 is essential for epithelial-to-mesenchymal transition in mammary epithelial cells A Kumar, J Xu, B Sung, S Kumar, D Yu, BB Aggarwal, K Mehta Breast Cancer Research 14 (1), 1-15 , 2012 2012 Citations: 81
Transglutaminase 2 reprogramming of glucose metabolism in mammary epithelial cells via activation of inflammatory signaling pathways S Kumar, TR Donti, N Agnihotri, K Mehta International journal of cancer 134 (12), 2798-2807 , 2014 2014 Citations: 73
Twist1 Activation in Muscle Progenitor Cells Causes Muscle Loss Akin to Cancer Cachexia AA Santosh Kumar, Parash Parajuli, Audrey Loumaye, Purba Singh, Sailaja ... Developmental Cell 45, 712–725 , 2018 2018 Citations: 63
Tissue transglutaminase, inflammation, and cancer: how intimate is the relationship? S Kumar, K Mehta Amino acids 44 (1), 81-88 , 2013 2013 Citations: 62
A Novel Triterpenoid Isolated from the Root Bark of Ailanthus excelsa Roxb (Tree of Heaven), AECHL-1 as a Potential Anti-Cancer Agent MS Lavhale, S Kumar, SH Mishra, SL Sitasawad PLoS One 4 (4), e5365 , 2009 2009 Citations: 57
E-pharmacophore guided discovery of pyrazolo [1, 5-c] quinazolines as dual inhibitors of topoisomerase-I and histone deacetylase G Joshi, S Kalra, UP Yadav, P Sharma, PK Singh, S Amrutkar, AJ Ansari, ... Bioorganic Chemistry 94, 103409 , 2020 2020 Citations: 41
Tissue transglutaminase expression promotes castration-resistant phenotype and transcriptional repression of androgen receptor AKTKM Amy Han, Santosh Kumar, Jansina Y. Fok Eur J Cancer 50 (9), 1685-96 , 2014 2014 Citations: 40
CAR T cell therapy: newer approaches to counter resistance and cost RK Yadav, A Ali, S Kumar, A Sharma, B Baghchi, P Singh, S Das, C Singh, ... Heliyon 6 (4) , 2020 2020 Citations: 34
Novel SUMO-Protease SENP7S Regulates β-catenin Signaling and Mammary Epithelial Cell Transformation. BKT Karami S, Lin FM, Kumar S, Bahnassy S, Thangavel H, Quttina M, Li Y, Ren J Scientific Reports 7 (46477) , 2017 2017 Citations: 32
Let-7a induces metabolic reprogramming in breast cancer cells via targeting mitochondrial encoded ND4 P Sharma, V Sharma, TS Ahluwalia, N Dogra, S Kumar, S Singh Cancer cell international 21 (1), 629 , 2021 2021 Citations: 29
Disruption of the PHRF1 tumor suppressor network by PML-RARα drives acute promyelocytic leukemia pathogenesis C Prunier, MZ Zhang, S Kumar, L Levy, O Ferrigno, G Tzivion, A Atfi Cell reports 10 (6), 883-890 , 2015 2015 Citations: 27
Steroids up-regulate p66Shc longevity protein in growth regulation by inhibiting its ubiquitination S Kumar, S Kumar, M Rajendran, SM Alam, FF Lin, PW Cheng, MF Lin PLoS One 6 (1), e15942 , 2011 2011 Citations: 27
Design, synthesis and anticancer activity of 2-arylimidazo [1, 2-a] pyridinyl-3-amines UP Yadav, AJ Ansari, S Arora, G Joshi, T Singh, H Kaur, N Dogra, ... Bioorganic Chemistry 118, 105464 , 2022 2022 Citations: 26