Joanne Soh Ern Chi
@shiga-med.ac.jp
Department of Biochemistry and Molecular Biology
Shiga University of Medical Science
A research scientist in the field of cardiovascular and kidney research
EDUCATION
PhD in Medical Science, Shiga University of Medical Science (SUMS), Japan
MSc in Molecular Medicine, UMBI, University of Kebangsaan Malaysia (UKM), Malaysia
BSc in Biotechnology (Hons), INTI International University, Malaysia
RESEARCH, TEACHING, or OTHER INTERESTS
General Biochemistry, Genetics and Molecular Biology, Molecular Medicine, Cancer Research, Cell Biology
Scopus Publications
Scholar Citations
Scholar h-index
Scholar i10-index
Scopus Publications
Joanne Ern Chi Soh, Akio Shimizu, Akira Sato, and Hisakazu Ogita
Elsevier BV
Joanne Ern Chi Soh, Akio Shimizu, Md Rasel Molla, Dimitar P. Zankov, Le Kim Chi Nguyen, Mahbubur Rahman Khan, Wondwossen Wale Tesega, Si Chen, Misa Tojo, Yoshito Ito,et al.
Elsevier BV
Md Rasel Molla, Akio Shimizu, Masahiro Komeno, Nor Idayu A. Rahman, Joanne Ern Chi Soh, Le Kim Chi Nguyen, Mahbubur Rahman Khan, Wondwossen Wale Tesega, Si Chen, Xiaoling Pang,et al.
Springer Science and Business Media LLC
AbstractWhether a small GTPase RhoA plays a role in the pathology of abdominal aortic aneurysm (AAA) has not been determined. We show here that RhoA expression is reduced in human AAA lesions, compared with normal areas. Furthermore, incidence of AAA formation is increased in vascular smooth muscle cell (VSMC)-specific RhoA conditional knockout (cKO) mice. The contractility of the aortic rings and VSMCs from RhoA cKO mice is reduced, and expression of genes related to the VSMC contractility is attenuated by loss of RhoA. RhoA depletion activates the mitogen-activated protein (MAP) kinase signaling, including MAP4K4, in the aorta and VSMCs. Inhibition of MAP4K4 activity by DMX-5804 decreases AAA formation. Set, a binding protein to active RhoA, functions as an activator of MAP4K4 by sequestering PP2A, an inhibitor of MAP4K4, in the absence of RhoA. In conclusion, RhoA counteracts AAA formation through inhibition of MAP4K4 in cooperation with Set.
Le Kim Chi Nguyen, Akio Shimizu, Joanne Ern Chi Soh, Masahiro Komeno, Akira Sato, and Hisakazu Ogita
Oxford University Press (OUP)
Abstract Transmembrane protein 168 (TMEM168) was found to be localized on the nuclear membrane. A heterozygous mutation (c.1616G>A, p. R539Q) in TMEM168 was identified in patients with Brugada syndrome. This mutation reduced expression of cardiomyocyte sodium channel Nav1.5 via Nedd4-2 E3 ubiquitin ligase-induced ubiquitination and degradation. However, the detailed molecular mechanism provoked by the TMEM168 mutant remains unclear. Here, we demonstrated that small heat shock protein αB-crystallin, which can bind to Nav1.5 and Nedd4-2 and interfere with the association of both proteins, was strongly recruited from the cell surface to the perinuclear region because of the much higher affinity of αB-crystallin with the TMEM168 mutant than with wild-type TMEM168. Following knockdown of αB-crystallin in HL-1 cardiomyocytes, the interaction of Nav1.5 with Nedd4-2 was increased, despite the reduced expression of Nav1.5. Moreover, reduction of Nav1.5 expression by αB-crystallin knockdown was rescued in the presence of a proteasome inhibitor MG-132, suggesting the importance of the αB-crystallin-modulated ubiquitin–proteasome system for the stability of Nav1.5 expression. Collectively, the balance of molecular interactions among Nav1.5, Nedd4-2 and αB-crystallin plays a role in the regulation of cardiomyocyte cell surface expression of Nav1.5, and the TMEM168 mutant disturbs this balance, resulting in a decrease in Nav1.5 expression.
Nor Idayu A. Rahman, Akira Sato, Khurelbaatar Tsevelnorov, Akio Shimizu, Masahiro Komeno, Mohammad Khusni Bin Ahmat Amin, Md Rasel Molla, Joanne Ern Chi Soh, Le Kim Chi Nguyen, Akinori Wada,et al.
American Association for Cancer Research (AACR)
Abstract The growth and progression of cancers are crucially regulated by the tumor microenvironment where tumor cells and stromal cells are mutually associated. In this study, we found that stomatin expression was markedly upregulated by the interaction between prostate cancer cells and stromal cells. Stomatin suppressed cancer cell proliferation and enhanced apoptosis in vitro and inhibited xenograft tumor growth in vivo. Stomatin inhibited Akt activation, which is mediated by phosphoinositide-dependent protein kinase 1 (PDPK1). PDPK1 protein stability was maintained by its binding to HSP90. Stomatin interacted with PDPK1 and interfered with the PDPK1–HSP90 complex formation, resulting in decreased PDPK1 expression. Knockdown of stomatin in cancer cells elevated Akt activation and promoted cell increase by promoting the interaction between PDPK1 and HSP90. Clinically, stomatin expression levels were significantly decreased in human prostate cancer samples with high Gleason scores, and lower expression of stomatin was associated with higher recurrence of prostate cancer after the operation. Collectively, these findings demonstrate the tumor-suppressive effect of stromal-induced stomatin on cancer cells. Significance: These findings reveal that interactions with stromal cells induce expression of stomatin in prostate cancer cells, which suppresses tumor growth via attenuation of the Akt signaling axis.
Masahiro Komeno, Xiaoling Pang, Akio Shimizu, Md Rasel Molla, Mako Yasuda-Yamahara, Shinji Kume, Nor Idayu A. Rahman, Joanne Ern Chi Soh, Le Kim Chi Nguyen, Mohammad Khusni B. Ahmat Amin,et al.
Elsevier BV
Nadiah Abu, Norahayu Othman, Nur’ Syahada Ab Razak, Nurul Ainaa’ Adilah Rus Bakarurraini, Siti Nurmi Nasir, Joanne Ern Chi Soh, Luqman Mazlan, Zairul Azwan Mohd Azman, and Rahman Jamal
Frontiers Media SA
Colorectal cancer (CRC) is one of the most widely diagnosed cancers worldwide. It has been shown that the body-mass index (BMI) of the patients could influence the tumor microenvironment, treatment response, and overall survival rates. Nevertheless, the mechanism on how BMI affects the tumorigenesis process, particularly the tumor microenvironment is still elusive. Herein, we postulate that extracellular vesicles (EVs) from CRC patients and non-CRC volunteers with different BMI could affect immune cells differently, in CD8 T cells particularly. We isolated the EVs from the archived serum of CRC patients with high and low BMI, as well as healthy controls with similar BMI status. The EVs were further characterized via electron microscopy, western blot and dynamic light scattering. Then, functional analysis was performed on CD8 T cells including apoptosis, cell proliferation, gene expression profiling and cytokine release upon co-incubation with the different EVs. Our results suggest that CRC-derived EVs were able to regulate the CD8 T cells. In some assays, low BMI EVs were functionally different than high BMI EVs. This study highlights the possible difference in the regulatory mechanism of cancer patients-derived EVs, especially on CD8 T cells.
Joanne EC Soh, Nadiah Abu, Ismail Sagap, Luqman Mazlan, Azyani Yahaya, Muaatamarulain Mustangin, Tze S Khoo, Sazuita Saidin, Muhiddin Ishak, Nurul S Ab Mutalib,et al.
Future Medicine Ltd
Colorectal cancer is the third commonest malignancy in Asia including Malaysia. The immunogenic cancer-testis antigens, which are expressed in a variety of cancers but with limited expression in normal tissues except the testis, represent an attractive approach to improve treatment options for colorectal cancer. We aimed to validate four PASD1 peptides as the immunotherapeutic targets in colorectal cancer. First, PASD1 mRNA and protein expression were determined via real-time polymerase chain reaction (RT-PCR) and immunohistochemistry. The PASD1 peptides specific to HLA-A*24:02 were investigated using IFN-y-ELISpot assay, followed by the cytolytic and granzyme-B-ELISpot assays to analyze the cytolytic effects of CD8+T cells. Gene and protein expressions of PASD1 were detected in 20% and 17.3% of colorectal cancer samples, respectively. PASD1(4) peptide was shown to be immunogenic in colorectal cancer samples. CD8+T cells raised against PASD1(4) peptide were able to lyze HLA-A*24:02+ PASD1+ cells. Our results reveal that PASD1(4) peptide represents a potential target for colorectal cancer.
Joanne Ern Chi Soh, Nadiah Abu, and Rahman Jamal
Future Medicine Ltd
The identification of cancer testis antigens (CTAs) has been an important finding in the search of potential targets for cancer immunotherapy. CTA is one of the subfamilies of the large tumor-associated antigens groups. It is aberrantly expressed in various types of human tumors but is absent in normal tissues except for the testis and placenta. This CTAs-restricted pattern of expression in human malignancies together with its potential immunogenic properties, has stirred the interest of many researchers to use CTAs as one of the ideal targets in cancer immunotherapy. To date, multiple studies have shown that CTAs-based vaccines can elicit clinical and immunological responses in different tumors, including colorectal cancer (CRC). This review details our current understanding of CTAs and CRC in regard to the expression and immunological responses as well as some of the critical hurdles in CTAs-based immunotherapy.