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Article ; Online: Response to the hunt for the perfect biomarker in nasopharyngeal carcinoma-the RRAS "race" beyond Epstein-barr virus?

Xiao, Ruowen / Mai, Shijuan

2022 Volume 8, Issue 6, Page(s) 2506–2507

Language	English
Publishing date	2022-01-15
Publishing country	China
Document type	Journal Article
ZDB-ID	2901601-0
ISSN	2219-6803 ; 2218-676X
ISSN (online)	2219-6803
ISSN	2218-676X
DOI	10.21037/tcr.2019.10.01
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Article ; Online: STRESS granule-associated RNA-binding protein CAPRIN1 drives cancer progression and regulates treatment response in nasopharyngeal carcinoma.

Yang, Te / Huang, Long / Qin, Haide / Mai, Shijuan

Medical oncology (Northwood, London, England)

2022 Volume 40, Issue 1, Page(s) 47

Abstract: Nasopharyngeal carcinoma (NPC) is a common malignancy of the head and neck that is mainly diagnosed in southern China and Southeast Asia, with a strong etiological link to Epstein‒Barr virus infection. Those with advanced-stage disease have a ... ...

Abstract	Nasopharyngeal carcinoma (NPC) is a common malignancy of the head and neck that is mainly diagnosed in southern China and Southeast Asia, with a strong etiological link to Epstein‒Barr virus infection. Those with advanced-stage disease have a significantly worse prognosis. There is an urgent need to identify novel therapeutic targets for the recurrent or metastatic nasopharyngeal carcinoma. With a particular focus on Cell Cycle Associated Protein 1 (CAPRIN1), one of the important RNA-binding proteints associated with stress granule formation, we used RT‒qPCR and immunohistochemistry to validate CAPRIN1 expression in NPC tissues and cell lines. Further, CAPRIN1 expression was knocked down using siRNA, and the effect on cell proliferation and migration was systematically assessed by in vitro assays. As a result, we demonstrated that CAPRIN1 was elevated in NPC compared to adjacent normal tissues. Knockdown of CAPRIN1 in NPC cells inhibited proliferation and migration, involving the regulation of cell cycle protein CCND2 and EMT signaling, respectively. Notably, we found that CAPRIN1 knockdown promoted cell apoptosis by regulation of the expression of apoptosis-related proteins cleaved-PARP and cleaved-Caspase3. Knockdown of CAPRIN1 increased NPC cell sensitivity to rapamycin, and increased NPC cell sensitivity to cisplatin and to X-rays. In conclusion, CAPRIN1 might drive NPC proliferation, regulate cell cycle and apoptosis, and affect tumor cell response to anti-cancer agents and X-ray irradiation. CAPRIN1 might serve as a potential target for NPC.
MeSH term(s)	Humans ; Nasopharyngeal Carcinoma/genetics ; Nasopharyngeal Carcinoma/drug therapy ; Nasopharyngeal Carcinoma/pathology ; Nasopharyngeal Neoplasms/genetics ; Nasopharyngeal Neoplasms/metabolism ; Nasopharyngeal Neoplasms/pathology ; Epstein-Barr Virus Infections/genetics ; Stress Granules ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Herpesvirus 4, Human ; Cell Proliferation ; Cell Cycle ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Cell Movement/genetics ; Cell Cycle Proteins/metabolism
Chemical Substances	RNA-Binding Proteins ; CAPRIN1 protein, human ; Cell Cycle Proteins
Language	English
Publishing date	2022-12-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	1201189-7
ISSN	1559-131X ; 0736-0118 ; 1357-0560
ISSN (online)	1559-131X
ISSN	0736-0118 ; 1357-0560
DOI	10.1007/s12032-022-01910-w
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Article ; Online: Identification and Validation of UPF1 as a Novel Prognostic Biomarker in Renal Clear Cell Carcinoma.

Wu, Chun / Li, Hongmu / Chang, Wuguang / Zhong, Leqi / Zhang, Lin / Wen, Zhesheng / Mai, Shijuan

Genes

2022 Volume 13, Issue 11

Abstract: Background: ...

Abstract	Background:
MeSH term(s)	Humans ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/pathology ; Prognosis ; RNA Helicases/genetics ; RNA Helicases/metabolism ; Kidney Neoplasms/genetics ; Kidney Neoplasms/pathology ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Tumor Microenvironment/genetics ; Trans-Activators/genetics ; Trans-Activators/metabolism
Chemical Substances	RNA Helicases (EC 3.6.4.13) ; RNA, Messenger ; UPF1 protein, human (EC 3.6.4.13) ; Trans-Activators
Language	English
Publishing date	2022-11-20
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes13112166
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Article ; Online: Identification of

Xiao, Ruowen / Shi, Lu / Yang, Te / Zhang, Meiyin / Wang, Huiyun / Mai, Shijuan

Translational cancer research

2022 Volume 8, Issue 2, Page(s) 664–675

Abstract: Background: Nasopharyngeal carcinoma (NPC) is a highly aggressive neoplasm mainly distributed in the eastern and southeastern parts of Asia. NPC has a poor prognosis among head and neck cancers, and molecular-targeted therapies showed limited clinical ... ...

Abstract	Background: Nasopharyngeal carcinoma (NPC) is a highly aggressive neoplasm mainly distributed in the eastern and southeastern parts of Asia. NPC has a poor prognosis among head and neck cancers, and molecular-targeted therapies showed limited clinical efficacy. Methods: We reviewed publications in the PubMed database and extracted genes associated with NPC. The online tool WebGestalt was used to perform Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis for these genes. Next, the two parameters, Jaccard Coefficient (JC) and Overlap Coefficient (OC), were used to analyze the crosstalk of each pair of selected pathways. The new NPC-related genes were predicted by protein-protein interaction (PPI) network combined with hub genes extraction. Western blotting, qRT-PCR, and immunohistochemistry (IHC) were used to detect the expression of candidate genes in NPC cells and tissues, and cellular function assays were used to explore the effects of genes on NPC cells. Results: A total of 552 genes were identified and used to build an NPC-related gene set (NPCgset). Pathways enriched in KEGG pathway analysis were further used for crosstalk analysis and were grouped into two modules: one was related to the carcinogenesis process, and the other was correlated with the immune response. Eight genes from the NPCgset were selected to build a PPI network, and two hub genes Conclusions: Our study may help to explore the biological processes underlying NPCgset and suggests that RRAS may act as a tumor suppressor gene in NPC.
Language	English
Publishing date	2022-01-15
Publishing country	China
Document type	Journal Article
ZDB-ID	2901601-0
ISSN	2219-6803 ; 2218-676X
ISSN (online)	2219-6803
ISSN	2218-676X
DOI	10.21037/tcr.2019.04.04
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Article ; Online: Ezetimibe Induces Paraptosis through Niemann-Pick C1-like 1 Inhibition of Mammalian-Target-of-Rapamycin Signaling in Hepatocellular Carcinoma Cells.

Yin, Yuting / Wu, Chun / Zhou, Yufeng / Zhang, Meiyin / Mai, Shijuan / Chen, Minshan / Wang, Hui-Yun

Genes

2023 Volume 15, Issue 1

Abstract: Currently, hepatocellular carcinoma (HCC) is characterized by its unfavorable prognosis and resistance to conventional chemotherapy and radiotherapy. Drug repositioning, an approach aimed at identifying novel therapeutic applications for existing drugs, ... ...

Abstract	Currently, hepatocellular carcinoma (HCC) is characterized by its unfavorable prognosis and resistance to conventional chemotherapy and radiotherapy. Drug repositioning, an approach aimed at identifying novel therapeutic applications for existing drugs, presents a cost-effective strategy for developing new anticancer agents. We explored the anticancer properties of Ezetimibe, a widely used oral lipid-lowering drug, in the context of HCC. Our findings demonstrate that Ezetimibe effectively suppresses HCC cell proliferation through paraptosis, an apoptotic-independent cell death pathway. The examination of HCC cells lines treated with Ezetimibe using light microscopy and transmission electron microscopy (TEM) showed cytoplasmic vacuolation in the perinuclear region. Notably, the nuclear membrane remained intact in both Ezetimibe-treated and untreated HCC cell lines. Probe staining assays confirmed that the cytoplasmic vacuoles originated from dilated endoplasmic reticulum (ER) compartments rather than mitochondria. Furthermore, a dose-dependent accumulation of reactive oxygen species (ROS) was observed in Ezetimibe-treated HCC cell lines. Co-treatment with the general antioxidant NAC attenuated vacuolation and improved cell viability in Ezetimibe-treated HCC cells. Moreover, Ezetimibe induced paraptosis through proteasome activity inhibition and initiation of the unfolded protein response (UPR) in HCC cell lines. In our in vivo experiment, Ezetimibe significantly impeded the growth of HCC tumors. Furthermore, when combined with Sorafenib, Ezetimibe exhibited a synergistic antitumor effect on HCC cell lines. Mechanistically, Ezetimibe induced paraptosis by targeting NPC1L1 to inhibit the PI3K/AKT/mTOR signaling pathway. In conclusion, our study highlights the potential of Ezetimibe as an anticancer agent by triggering paraptosis in HCC cells.
MeSH term(s)	Animals ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Liver Neoplasms/drug therapy ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Sirolimus ; Ezetimibe/pharmacology ; Ezetimibe/therapeutic use ; Paraptosis ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Cell Line, Tumor ; Signal Transduction ; Mammals/metabolism
Chemical Substances	Sirolimus (W36ZG6FT64) ; Ezetimibe (EOR26LQQ24) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
Language	English
Publishing date	2023-12-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes15010004
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Article ; Online: Overexpression of PSAT1 is Correlated with Poor Prognosis and Immune Infiltration in Non-Small Cell Lung Cancer.

Li, Hongmu / Wu, Chun / Chang, Wuguang / Zhong, Leqi / Gao, Wuyou / Zeng, Mingyue / Wen, Zhesheng / Mai, Shijuan / Chen, Youfang

Frontiers in bioscience (Landmark edition)

2023 Volume 28, Issue 10, Page(s) 243

Abstract: Purpose: Current evidence suggests that phosphoserine aminotransferase 1 (: Methods: The expression profile of : Results: Analysis of transcriptional expression profiles using TCGA data revealed overexpression of : Conclusions: ... ...

Abstract	Purpose: Current evidence suggests that phosphoserine aminotransferase 1 ( Methods: The expression profile of Results: Analysis of transcriptional expression profiles using TCGA data revealed overexpression of Conclusions: PSAT1
MeSH term(s)	Humans ; Carcinoma, Non-Small-Cell Lung/genetics ; Cell Line ; Cell Proliferation/genetics ; Immunotherapy ; Lung Neoplasms/genetics ; Tumor Microenvironment/genetics
Chemical Substances	PSAT1 protein, human (EC 2.6.1.52)
Language	English
Publishing date	2023-11-02
Publishing country	Singapore
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2704569-9
ISSN	2768-6698 ; 2768-6698
ISSN (online)	2768-6698
ISSN	2768-6698
DOI	10.31083/j.fbl2810243
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Article ; Online: Two somatic mutations in the androgen receptor N-terminal domain are oncogenic drivers in hepatocellular carcinoma.

Ren, Qian-Nan / Huang, Dan-Hui / Zhang, Xiao-Nan / Wang, Yue-Ning / Zhou, Yu-Feng / Zhang, Mei-Yin / Wang, Shuo-Cheng / Mai, Shi-Juan / Wu, De-Hua / Wang, Hui-Yun

Communications biology

2024 Volume 7, Issue 1, Page(s) 22

Abstract: The androgen receptor (AR) plays an important role in male-dominant hepatocellular carcinoma, and specific acquired somatic mutations of AR have been observed in HCC patients. Our previous research have established the role of AR wild type as one of the ... ...

Abstract	The androgen receptor (AR) plays an important role in male-dominant hepatocellular carcinoma, and specific acquired somatic mutations of AR have been observed in HCC patients. Our previous research have established the role of AR wild type as one of the key oncogenes in hepatocarcinogenesis. However, the role of hepatic acquired somatic mutations of AR remains unknown. In this study, we identify two crucial acquired somatic mutations, Q62L and E81Q, situated close to the N-terminal activation function domain-1 of AR. These mutations lead to constitutive activation of AR, both independently and synergistically with androgens, making them potent driver oncogene mutations. Mechanistically, these N-terminal AR somatic mutations enhance de novo lipogenesis by activating sterol regulatory element-binding protein-1 and promote glycogen accumulation through glycogen phosphorylase, brain form, thereby disrupting the AMPK pathway and contributing to tumorigenesis. Moreover, the AR mutations show sensitivity to the AMPK activator A769662. Overall, this study establishes the role of these N- terminal hepatic mutations of AR as highly malignant oncogenic drivers in hepatocarcinogenesis and highlights their potential as therapeutic targets for patients harboring these somatic mutations.
MeSH term(s)	Humans ; Male ; AMP-Activated Protein Kinases ; Carcinogenesis/genetics ; Carcinoma, Hepatocellular/genetics ; Liver Neoplasms/genetics ; Mutation ; Receptors, Androgen/genetics
Chemical Substances	AMP-Activated Protein Kinases (EC 2.7.11.31) ; Receptors, Androgen ; AR protein, human
Language	English
Publishing date	2024-01-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-023-05704-2
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Article ; Online: TRIM29 modulates proteins involved in PTEN/AKT/mTOR and JAK2/STAT3 signaling pathway and suppresses the progression of hepatocellular carcinoma.

Yin, Yu-Ting / Shi, Lu / Wu, Chun / Zhang, Mei-Yin / Li, Jia-Xin / Zhou, Yu-Feng / Wang, Shuo-Cheng / Wang, Hui-Yun / Mai, Shi-Juan

Medical oncology (Northwood, London, England)

2024 Volume 41, Issue 3, Page(s) 79

Abstract: Tripartite motif-containing 29 (TRIM29), also known as the ataxia telangiectasia group D-complementing (ATDC) gene, has been reported to play an oncogenic or tumor suppressive role in developing different tumors. So far, its expression and biological ... ...

Abstract	Tripartite motif-containing 29 (TRIM29), also known as the ataxia telangiectasia group D-complementing (ATDC) gene, has been reported to play an oncogenic or tumor suppressive role in developing different tumors. So far, its expression and biological functions in hepatocellular carcinoma (HCC) remain unclear. We investigated TRIM29 expression pattern in human HCC samples using quantitative RT-PCR and immunohistochemistry. Relationships between TRIM29 expression level, clinical prognostic indicators, overall survival (OS), and disease-free survival (DFS) were evaluated by Kaplan-Meier analysis and Cox proportional hazards model. A series of in vitro experiments and a xenograft tumor model were conducted to detect the functions of TRIM29 in HCC cells. RNA sequencing, western blotting, and immunochemical staining were performed to assess the molecular regulation of TRIM29 in HCC. We found that the mRNA and protein levels of TRIM29 were significantly reduced in HCC samples, compared with adjacent noncancerous tissues, and were negatively correlated with poor differentiation of HCC tissues. Survival analysis confirmed that lower TRIM29 expression significantly correlated with shorter OS and DFS of HCC patients. TRIM29 overexpression remarkably inhibited cell proliferation, migration, and EMT in HCC cells, whereas knockdown of TRIM29 reversed these effects. Moreover, deactivation of the PTEN/AKT/mTOR and JAK2/STAT3 pathways might be involved in the tumor suppressive role of TRIM29 in HCC. Our findings indicate that TRIM29 in HCC exerts its tumor suppressive effects through inhibition of the PTEN/AKT/mTOR and JAK2/STAT3 signaling pathways and may be used as a potential biomarker for survival in patients with HCC.
MeSH term(s)	Humans ; Carcinoma, Hepatocellular/pathology ; Cell Line, Tumor ; Cell Movement/genetics ; Cell Proliferation/genetics ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation, Neoplastic ; Janus Kinase 2 ; Liver Neoplasms/pathology ; Proto-Oncogene Proteins c-akt/metabolism ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism ; Signal Transduction ; STAT3 Transcription Factor ; TOR Serine-Threonine Kinases/metabolism ; Transcription Factors/genetics ; Animals
Chemical Substances	DNA-Binding Proteins ; JAK2 protein, human (EC 2.7.10.2) ; Janus Kinase 2 (EC 2.7.10.2) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; PTEN protein, human (EC 3.1.3.67) ; STAT3 protein, human ; STAT3 Transcription Factor ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Transcription Factors ; TRIM29 protein, human
Language	English
Publishing date	2024-02-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	1201189-7
ISSN	1559-131X ; 0736-0118 ; 1357-0560
ISSN (online)	1559-131X
ISSN	0736-0118 ; 1357-0560
DOI	10.1007/s12032-024-02307-7
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Article ; Online: PD1

Wu, Chun / Duan, Lianhui / Li, Hongmu / Liu, Xuefei / Cai, Taonong / Yang, Yang / Yin, Yuting / Chang, Wuguang / Zhong, Leqi / Zhang, Lin / Cheng, Yixin / Qin, Haide / Wen, Zhesheng / Wang, Huiyun / Mai, Shijuan

Clinical and translational medicine

2023 Volume 13, Issue 6, Page(s) e1303

Abstract: Background: Bladder cancer (BLCA) is one of the most diagnosed cancers in humans worldwide. Recently, immunotherapy has become a main treatment option for BC. However, most BLCA patients do not respond to immune checkpoint inhibitors or relapse after ... ...

Abstract	Background: Bladder cancer (BLCA) is one of the most diagnosed cancers in humans worldwide. Recently, immunotherapy has become a main treatment option for BC. However, most BLCA patients do not respond to immune checkpoint inhibitors or relapse after immunotherapy. Therefore, it is very important to identify novel biomarkers for the prediction of immunotherapy response in B patients. Methods: Pancancer single-cell RNA sequencing (scRNA-seq) data were used to identify the clusters of CD4 Results: This study identified two novel exhausted CD4 Conclusions: PD1
MeSH term(s)	Humans ; Epithelial-Mesenchymal Transition ; T-Lymphocytes ; Neoplasm Recurrence, Local ; Urinary Bladder Neoplasms/therapy ; CD4-Positive T-Lymphocytes ; Tumor Microenvironment ; Methyltransferases
Chemical Substances	METTL3 protein, human (EC 2.1.1.62) ; Methyltransferases (EC 2.1.1.-)
Language	English
Publishing date	2023-06-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2697013-2
ISSN	2001-1326 ; 2001-1326
ISSN (online)	2001-1326
ISSN	2001-1326
DOI	10.1002/ctm2.1303
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Article: Combination Treatment With Inhibitors of ERK and Autophagy Enhances Antitumor Activity of Betulinic Acid in Non-small-Cell Lung Cancer

Sun, Chao-Yue / Cao, Di / Ren, Qian-Nan / Zhang, Shan-Shan / Zhou, Ning-Ning / Mai, Shi-Juan / Feng, Bing / Wang, Hui-Yun

Frontiers in pharmacology

2021 Volume 12, Page(s) 684243

Abstract: Aberrant activation of the Ras-ERK signaling pathway drives many important cancer phenotypes, and several inhibitors targeting such pathways are under investigation and/or approved by the FDA as single- or multi-agent therapy for patients with melanoma ... ...

Abstract	Aberrant activation of the Ras-ERK signaling pathway drives many important cancer phenotypes, and several inhibitors targeting such pathways are under investigation and/or approved by the FDA as single- or multi-agent therapy for patients with melanoma and non-small-cell lung cancer (NSCLC). Here, we show that betulinic acid (BA), a natural pentacyclic triterpenoid, inhibits cell proliferation, and induces apoptosis and protective autophagy in NSCLC cells. Thus, the cancer cell killing activity of BA is enhanced by autophagy inhibition. Mitogen-activated protein kinases, and especially ERK that facilitates cancer cell survival, are also activated by BA treatment. As such, in the presence of ERK inhibitors (ERKi), lung cancer cells are much more sensitive to BA. However, the dual treatment of BA and ERKi results in increased protective autophagy and AKT phosphorylation. Accordingly, inhibition of AKT has a highly synergistic anticancer effect with co-treatment of BA and ERKi. Notably, autophagy inhibition by hydroxychloroquine (HCQ) increases the response of lung cancer cells to BA in combination with ERKi.
Language	English
Publishing date	2021-06-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2021.684243
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