NUPR1 promotes the proliferation and metastasis of oral squamous cell carcinoma cells by activating TFE3-dependent autophagy

Fan, Teng-Fei; Wang, Xiaoning; Zhang, Sheng; Deng, Ping; Jiang, Yi; Liang, Yaxuan; Jie, Sheng; Wang, Qing; Li, Chuwen; Tian, Guocai; Zhang, Zhen; Ren, Zhenhu; Li, Bo; Chen, Yanrong; He, Zhijing; Luo, Yan; Chen, Mingliang; Wu, Hanjiang; Yu, Zhengping; Pi, Huifeng; Zhou, Zhou; Zhang, Zhiyuan

doi:10.1038/s41392-022-00939-7

Cited by 65 publications

(26 citation statements)

References 32 publications

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“…ERK phosphorylation modulates autophagy [31,32], and autophagy has been shown to be associated with cell proliferation in cancer cells [33]. Therefore, we speculated that ANGPTL8-mediated activation of the ERK pathway could promote HCC cell proliferation via autophagy.…”

Section: Discussionmentioning

confidence: 95%

Dual role of ANGPTL8 in promoting tumor cell proliferation and immune escape during hepatocarcinogenesis

Guo¹,

Gao²,

Yuan³

et al. 2023

Preprint

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The interplay between hepatocellular carcinoma (HCC) cells and the tumor microenvironment is essential for hepatocarcinogenesis, but their contributions to HCC development are incompletely understood. We assessed the role of ANGPTL8, a protein secreted by HCC cells, in hepatocarcinogenesis and the mechanisms through which ANGPTL8 mediates crosstalk between HCC cells and tumor-associated macrophages. Immunohistochemical, Western blotting, RNA-Seq and Flow cytometry analysis of ANGPTL8 were performed. A series of in vitro and in vivo experiments were conducted to reveal the role of ANGPTL8 in the progression of HCC. ANGPTL8expression was positively correlated with tumor malignancy in HCC, and high ANGPTL8 expression was associated with poor overall survival (OS) and disease-free survival (DFS). ANGPTL8 promoted HCC cell proliferation in vitro and in vivo, and ANGPTL8KO inhibited the development of HCC in both DEN-induced and DEN-plus-CCL4-induced mouse HCC tumors. Mechanistically, the ANGPTL8–LILRB2/PIRB interaction promoted polarization of macrophages to the immunosuppressive M2 phenotype in macrophages and recruiting immunosuppressive T cells. In hepatocytes, ANGPTL8-mediated stimulation of LILRB2/PIRB regulated the ROS/ERK pathway and upregulated autophagy, leading to proliferation of HCC cells. Our data support that ANGPTL8 has dual role of in promoting tumor cell proliferation and immune escape during hepatocarcinogenesis.

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Section: Discussionmentioning

confidence: 95%

Dual role of ANGPTL8 in promoting tumor cell proliferation and immune escape during hepatocarcinogenesis

Guo¹,

Gao²,

Yuan³

et al. 2023

Preprint

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“…Several studies have reported that NUPR1 is associated with autophagy [24] . Hence, we speculated that NUPR1 may be also implicated in modulating autophagy in CC cells.…”

Section: Resultsmentioning

confidence: 99%

MicroRNA-3137/Nuclear Protein Transcription Regulator 1 Axis Regulates Cervical Cancer Cells Proliferation Apoptosis and Autophagy by PI3K/AKT/mTOR pathway

Xing¹,

Zhang²,

Cai³

2022

IJPS

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Cervical cancer belongs to the second most frequent kind of cancer in female as well as a major cause of mortality in female all over the world. MicroRNAs are crucial modulators of multiple diseases. Based on GSE86100 database, microRNA-3137 expression was low in cervical cancer tissues and the difference was most significant, thus we further probed the potential along with mechanism of microRNA-3137 in cervical cancer cells. Reverse transcription-quantitative polymerase chain reaction together with Western blot was implemented for examining gene expression. 5-ethynyl-2'-deoxyuridine and flow cytometry analyses were adopted for assessing cervical cancer cells proliferation and apoptosis. Immunofluorescence was implemented to measure the fluorescence intensity of autophagy marker LC3II. Target scan together with luciferase reporter assay were implemented for confirming the direct binding of microRNA-3137 and nuclear protein transcriptional regulator 1. The results revealed that, microRNA-3137 was under expressed in cervical cancer cells. Overexpressed microRNA-3137 repressed cervical cancer cells proliferation while elevated cells apoptosis. Besides, nuclear protein transcriptional regulator 1 was directly targeted and negatively regulated by microRNA-3137 and was highly expressed in cervical cancer cells. Moreover, nuclear protein transcriptional regulator 1 silence promoted autophagy in cervical cancer cells and rescue assays further validated that the microRNA-3137/nuclear protein transcriptional regulator 1 axis suppressed cervical cancer cells proliferation while promoted cells apoptosis and autophagy through inactivation of the phosphatidylinositol-3-kinase/ protein kinase B/mammalian target of rapamycin pathway. Collectively, our study demonstrated that microRNA-3137/nuclear protein transcriptional regulator 1 axis affected cervical cancer cells proliferation, apoptosis, along with autophagy by means of inhibiting the phosphatidylinositol-3-kinase/protein kinase B/ mammalian target of rapamycin pathway, which may offer novel insights into the mechanism of cervical cancer progression as well as a novel therapy targeting for cervical cancer therapy. Key words: Cervical cancer, microRNA-3137, nuclear protein transcriptional regulator 1, autophagy, phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin pathwayThis is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms This article was originally published in a special issue, "Current Trends in Pharmaceutical and Biomedical Sciences"

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“…In the past decade, the occurrence of oral cancer has increased markedly worldwide ( 17 ). OSCC, a common type of oral cancer, has been characterized by a high degree of malignancy and poor prognosis ( 18 ). It has been shown that OSCC has high a potential for metastasis ( 19 ).…”

Section: Discussionmentioning

confidence: 99%

COL4A1 promotes the proliferation and migration of oral squamous cell carcinoma cells by binding to NID1

Tian

Sun

et al. 2023

Exp Ther Med

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Collagen type IV α1 chain (COL4A1) is a collagen protein that acts as a tumor-promoting factor in several types of cancer. However, the role and the potential mechanisms involving COL4A1 in oral squamous cell carcinoma (OSCC) remain unclear. Using reverse transcription-quantitative PCR and western blotting, the expression levels of COL4A1 and (nidogen-1) NID1 in OSCC cells were assessed. Cell Counting Kit-8, EdU staining and colony formation assays were used to evaluate cell proliferation. Cell migration and invasion were assessed using wound healing and Transwell invasion assays, respectively. The expression levels of proteins involved in epithelial-mesenchymal transition (EMT) were assessed using western blotting. In addition, the association between COL4A1 and NID1 was analyzed using TNMplot and the STRING database and verified by co-immunoprecipitation analysis. COL4A1 expression was found to be significantly increased in OSCC cells. Knockdown of COL4A1 expression decreased SCC-4 cell proliferation, migration and invasion, as well as the progression of EMT. In addition, COL4A1 was shown to be significantly positively associated with NID1 in OSCC and to bind to NID1. NID1 overexpression reversed the inhibitory effects of COL4A1 knockdown on cell proliferation, migration and invasion as well as on the progression of EMT in OSCC cells. In summary, the present findings demonstrated that COL4A1 promoted cell proliferation and migration as well as the progression of EMT in OSCC cells by binding to NID1, highlighting a potential avenue for therapeutic management of OSCC.

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NUPR1 promotes the proliferation and metastasis of oral squamous cell carcinoma cells by activating TFE3-dependent autophagy

Cited by 65 publications

References 32 publications

Dual role of ANGPTL8 in promoting tumor cell proliferation and immune escape during hepatocarcinogenesis

Dual role of ANGPTL8 in promoting tumor cell proliferation and immune escape during hepatocarcinogenesis

MicroRNA-3137/Nuclear Protein Transcription Regulator 1 Axis Regulates Cervical Cancer Cells Proliferation Apoptosis and Autophagy by PI3K/AKT/mTOR pathway

COL4A1 promotes the proliferation and migration of oral squamous cell carcinoma cells by binding to NID1

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