Jia Ma

Chinese Academy of Medical Sciences & Peking Union Medical College

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Jun Xia

Hangzhou Medical College

Zhiwei Wang

Bengbu Medical College

Tong Cao

First Affiliated Hospital of Bengbu Medical College

Jia Li

Chinese Center For Disease Control and Prevention

Yuyun Li

Guangdong Medical College

Z. Peter Wang

Massachusetts General Hospital

Miaomiao Zhang

First Affiliated Hospital of Xi'an Jiaotong University

Jialei Hu

Zhejiang University

Ying Shi

Hunan Cancer Hospital

Fanpeng Zeng

Xuzhou Central Hospital

Cooperative Institutions

Bengbu Medical College

Huazhong University of Science and Technology

Union Hospital

Chinese Academy of Sciences

Sun Yat-sen University

Chinese Academy of Medical Sciences & Peking Union Medical College

Sichuan University

First Affiliated Hospital of Xi'an Jiaotong University

Capital Medical University

Dalian Medical University

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FBXO31 is upregulated by METTL3 to promote pancreatic cancer progression via regulating SIRT2 ubiquitination and degradation

Cell Death and Disease (2024)

Kai Chen Yue Wang Xingna Dai Jingjing Luo Shangshang Hu

Abstract FBXO31, a member of F-box family to comprise of SCF complex, contributes to a pivotal role in cancer progression. However, the possible involvements of FBXO31 in PC are unelucidated. Here, we reported that FBXO31 was overexpressed in PC patients, which was negatively associated with survival in PC patients. Furthermore, FBXO31 significantly enhanced growth, migration and invasion of PC cells in vitro. Consistently, FBXO31 overexpression promoted tumor growth in nude mice. Mechanistically, SIRT2 was a target of FBXO31 and interacted with FBXO31. Protein half-life and ubiquitination analysis demonstrated that FBXO31 promoted proteasome-dependent degradation of SIRT2. In addition, FBXO31 binds to sirtuin-type domain of SIRT2. Moreover, SIRT2 is required for the oncogenic role of FBXO31 in PC progression. Impressively, METTL3 induced m6A modification of FBXO31 and up-regulated FBXO31 expression, subsequently leading to SIRT2 down-regulation in PC cells. The results showed that METTL3 enhanced FBXO31 mRNA translation in YTHDF1-dependent manner. Taken together, we suggest that METTL3–FBXO31–SIRT2 axis was involved in PC tumorigenesis, which could identify new targets for PC treatment.

SIRT2

10.1038/s41419-024-06425-y

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Citations (4)

Role of OCT2 and MATE1 in renal disposition and toxicity of nitidine chloride

British Journal of Pharmacology (2016)

L P Li Feifeng Song Yayun Weng Xiaoe Yang K Wang

Background and Purpose Nitidine chloride (NC), a benzophenanthridine alkaloid, has various biological properties including anticancer and analgesic activities. The aim of the present study was to evaluate the role of organic cation transporter 2 (OCT2) and multidrug and toxin extrusion 1 (MATE1) in the renal disposition and nephrotoxicity of NC. Experimental Approach MDCK cells stably expressing human OCT2 and/or hMATE1 were used to investigate the OCT2‐ and MATE1‐mediated transport of NC. In addition, the accumulation of NC and its potential toxicity were studied in rat primary‐cultured proximal tubular (rPCPT) cells and in rats in vivo . Key Results NC was found to be a high‐affinity substrate of both OCT2 and MATE1 with high cytotoxicity in MDCK‐hOCT2/hMATE1 and MDCK‐hOCT2 compared to mock cells. The OCT2 inhibitors, cimetidine and (+)‐tetrahydropalmatine ((+)‐THP), significantly reduced NC accumulation and cytotoxicity in MDCK‐hOCT2, MDCK‐hOCT2/hMATE1 and rPCPT cells. Severe kidney damage with high levels of blood urea nitrogen and lactate dehydrogenase (LDH), reduced levels of alkaline phosphatase (ALP) and pathological changes were found in rats after 20 days of successive i.v. doses of NC (5 mg·kg −1 ·day −1 ). Concomitantly, the concentration of NC in the kidney reached similar high levels at 2 h after the last dose of the 20 day treatment as those observed at 0.5 h after a single i.v. dose of 5 mg·kg −1 . Conclusions and Implications Our data indicate that NC‐induced nephrotoxicity might be mainly attributed to OCT2‐mediated extensive renal uptake and weak tubular secretion by MATE1.

Nephrotoxicity

Blood urea nitrogen

10.1111/bph.13537

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Citations (34)

miR-7 Suppresses Tumor Progression by Directly Targeting MAP3K9 in Pancreatic Cancer

Molecular Therapy — Nucleic Acids (2018)

Jun Xia Tong Cao Cong Ma Yongyong Shi Yu Sun

Tumor progression

10.1016/j.omtn.2018.08.012

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Citations (50)

FOXA1 overexpression suppresses interferon signaling and immune response in cancer

Carolina Digital Repository (University of North Carolina at Chapel Hill) (2021)

Yongfei He Liang Wang Tao Wei Yun Xiao Sheng Hu

FOXA1

10.17615/pg5w-dx64

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MicroRNA-124 regulates the radiosensitivity of non-small cell lung cancer cells by targeting TXNRD1

Oncology Letters (2017)

Chuncheng Hao Xiangying Xu Jia Ma Jun Xia Bingbing Dai

Radiation treatment remains one of the major modalities in the treatment of lung cancer. Although the majority of patients initially respond to treatment with radiation, resistance inevitably develops and leads to treatment failure. Therefore, the identification of the underlying molecular mechanisms of radiation resistance may facilitate the development of novel approaches for overcoming resistance, and enhance the efficacy of treatment with radiation in lung and other types of cancer. In the present study we established three radiation‑resistant sub‑cell lines derived from the radiation‑sensitive lung cancer cell line HCC827. Using a polymerase chain reaction microRNA (miRNA) array, multiple miRNAs were identified to be markedly downregulated in radiation‑resistant cells, including miRNA (miR)‑124, miR‑191 and miR‑205. It was observed that overexpression of miR‑124 sensitized the resistant cells to treatment with radiation and that thioredoxin reductase 1 (TXNRD1) is a novel target of miR‑124. Furthermore, it was demonstrated that knockdown of TXNRD1 using small interfering RNA increased the basal level of reactive oxygen species and sensitized the cells to radiation treatment. The results of the present study demonstrated that multiple miRNAs are downregulated in radiation-resistant lung cancer cells and that downregulation of miR-124 mediates radiation resistance through the targeting of TXNRD1 mRNA expression. The present study revealed a novel molecular mechanism of miRNA‑mediated radiation resistance and identified miR-124-regulated TXNRD1 as a novel therapeutic target for overcoming radiation resistance in the treatment of lung cancer.

Radiosensitivity

10.3892/ol.2017.5701

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Citations (30)

Functional Role of miR-34 Family in Human Cancer

Current Drug Targets (2013)

Rui Wang Jia Ma Qiong Wu Jun Xia Lucio Miele

Recently, microRNAs (miRNAs) including miR-34 family have been found to play a critical role in tumorigenesis through regulating the expression of its target genes, which are involved in many cellular processes such as cell proliferation, survival, apoptosis, migration, invasion and angiogenesis. Thus, this review described the role of miR-34 family and how its deregulation is involved in the development and progression of human malignances. Moreover, we described the potential role of miR-34 as a novel biomarker for tumor diagnosis. Furthermore, we summarized that miR-34 family could be up-regulated by natural compounds in human cancers. Therefore, targeting miR-34 family could be a novel strategy for achieving better treatment outcome of cancer patients in the future. Keywords: miR-34, cancer, natural compound, oncogene, therapy, tumor suppressor gene.

10.2174/13894501113149990191

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Citations (43)

BMP4 overexpression induces the upregulation of APP/Tau and memory deficits in Alzheimer’s disease

Cell Death Discovery (2021)

Xiaoqing Zhang Juan Li Li Ma Hui Xu Yun Cao

Abstract Alzheimer’s disease (AD) is a chronic progressive degenerative disease of the nervous system. Its pathogenesis is complex and is related to the abnormal expression of the amyloid β (Aβ), APP, and Tau proteins. Evidence has demonstrated that bone morphogenetic protein 4 (BMP4) is highly expressed in transgenic mouse models of AD and that endogenous levels of BMP4 mainly affect hippocampal function. To determine whether BMP4 participates in AD development, transgenic mice were constructed that overexpress BMP4 under the control of the neuron-specific enolase (NSE) promoter. We also performed MTT, FACS, transfection, TUNEL, and Western blotting assays to define the role of BMP4 in cells. We found that middle-aged BMP4 transgenic mice exhibited impaired memory via the Morris water maze experiment. Moreover, their hippocampal tissues exhibited high expression levels of AD-related proteins, including APP, Aβ, PSEN-1, Tau, P-Tau (Thr181), and P-Tau (Thr231). Furthermore, in multiple cell lines, the overexpression of BMP4 increased the expression of AD-related proteins, whereas the downregulation of BMP4 demonstrated opposing effects. Consistent with these results, BMP4 modulation affected cell apoptosis via the regulation of BAX and Bcl-2 expression in cells. Our findings indicate that BMP4 overexpression might be a potential factor to induce AD.

10.1038/s41420-021-00435-x

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Citations (19)

Research Progress on the Readout Circuit of Superconducting Single-Photon Detectors

2022 7th International Conference on Integrated Circuits and Microsystems (ICICM) (2024)

Jia Ma Wenjuan Hu Fei Yuan Qiang Xü Haizhi Song

Photon Counting

10.1109/icicm63644.2024.10814227

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[The effects of tissue inhibitor of metalloproteinases on beta-dystroglycan in salivary adenoid cystic carcinoma].

PubMed (2013)

Yanmei Hao Jia Ma Chenchen Si Jia Xu Jing Jie

To investigate the expression of beta-dystroglycan (beta-DG) and the roles of tissue inhibitor of metalloproteinases (TIMPs) on beta-DG in salivary adenoid cystic carcinoma (SACC).beta-DG in highly lung metastatic cell line ACC-M and lowly lung metastatic one ACC-2 was tested by immunocytochemistry with different concentrations (10, 15, 20, 25 micromol x L(-1)) of TIMPs, and that without the regulation of TIMPs was served as controls. beta-DG was detected in seven specimens of SACC and ten cases of normal salivary gland tissues which were considered as a comparison group by immunohistochemistry.There was no positive beta-DG immune-staining at the ACC-2 and ACC-M cell lines without TIMPs in the cell culture. beta-DG expressed after the regulation of TIMPs. beta-DG expression was localized predominantly in basement membrane of the acinus, while the negative results were distributed in the carcinoma cells and around the cancer cell nests.Beta-DG is widely expressed by transmembrane protein that plays important roles in connecting the extracellular matrix to the cytoskeleton, the fracture of this structure means that it is easy to invade and transfer, so restoration of beta-DG expression by TIMPs is considered to be critical for successful treatment of SACC.

Adenoid Cystic Carcinoma

BETA (programming language)

Dystroglycan

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Arsenic trioxide activates yes-associated protein by lysophosphatidic acid metabolism to selectively induce apoptosis of vascular smooth muscle cells

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research (2022)

Hongchi Yu Zhé Hóu Maolong Xiang Fan Yang Jia Ma

Arsenic Trioxide

Probucol

10.1016/j.bbamcr.2022.119211

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Citations (11)