MicroRNA‑107 may regulate lung cancer cell proliferation and apoptosis by targeting TP53 regulated inhibitor of apoptosis 1

Cai, Peng; Li, Jingjing; Chen, Guiming; Peng, Bing; Yu, Liuyang; Zhao, Bolin; Yu, Yi

doi:10.3892/ol.2020.11248

Cited by 8 publications

(10 citation statements)

References 33 publications

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“…TRIAP1 also increased the risk of recurrence or metastasis in afflicted patients with non-small cell lung cancer (NSCLC) following irradiation [ 14 ]. Knockdown of TRIAP1 inhibited the ability of proliferation, apoptosis, migration and invasion of thyroid cancer, oral squamous cell carcinoma (OSCC) and Lung cancer cells [ 34 – 36 ]. In our study, we revealed that TRIAP1 was highly expressed in PCa tissues, and the expression of TRIAP1 was negatively correlated with the expression of miR-506-3p and positively correlated with the expression of PCGEM1.…”

Section: Discussionmentioning

confidence: 99%

PCGEM1 promotes proliferation, migration and invasion in prostate cancer by sponging miR-506 to upregulate TRIAP1

Li¹,

Li³

et al. 2022

BMC Urol

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Background The important role of long noncoding RNAs (lncRNAs) in cancer has been demonstrated in many studies. Prostate cancer gene expression marker 1 (PCGEM1) is a lncRNA specifically expressed within the prostate and overexpressed in many cancer cells. Numerous studies have shown that PCGEM1 promotes cell proliferation, invasion and migration. However, the specific mechanism of PCGEM1 within prostate cancer (PCa) has not been elucidated. MicroRNA-506-3p (miR-506-3p) is a noncoding RNA, and studies have indicated that miR-506-3p is downregulated in prostate cancer cell lines and functions as a tumor suppressor. Methods The TCGA (GEPIA) database (http://gepia.cancer-pku.cn/) was employed to measure PCGEM1 levels in PCa. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine the PCGEM1 gene level. CCK-8 (Cell Counting Kit-8) and colony formation assays were used to detect cell proliferation, and Transwell assays were applied to assess cell invasion and migration. The interacting ability of miR-506-3p with PCGEM1 or TRIAP1 was validated through a dual-luciferase reporter assay. TRIAP1 protein expression was detected by Western blotting. Results PCGEM1 expression was increased in PCa tissues and cells. In PCa tissues, High PCGEM1 expression was associated with high Gleason score, distant metastasis and extracapsular extension. In addition, PCGEM1 knockdown inhibited PCa cell (C4-2B and PC-3) proliferation, invasion and migration. miR-506-3p may interact with PCGEM1 or TRIAP1, and the suppressive effect of PCGEM1 knockdown was reversed when TRIAP1 or a miR-506-3p inhibitor was cotransfected. Conclusion PCGEM1 expression increased in PCa cells and tissues, enhancing PCa cell proliferation, migration and invasion by sponging miR-506 to upregulate TRIAP1.

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Section: Discussionmentioning

confidence: 99%

PCGEM1 promotes proliferation, migration and invasion in prostate cancer by sponging miR-506 to upregulate TRIAP1

Li¹,

Li³

et al. 2022

BMC Urol

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“…In terms of PCNA expression regulation, we noticed a suppression of miR-107, as well as a promotion of ROCK1 on PCNA expression in ox-LDL-induced VSMCs. Furthermore, PCNA together with cyclin D1 could be significantly decreased with miR-107 ectopic expression in lung cancer cells and colorectal cancer cells [ 39 , 40 ], suggesting that miR-107 was an important regulator of cell proliferation. MMP2, MMP9, PCNA, ROCK1, and ROCK2 were increased in a mouse model of AS, and the receptor antagonist of IL-8, playing a key part in VSMCs proliferation and migration, could suppress the development of AS by inhibiting ROCKs [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

Blocking circ_UBR4 suppressed proliferation, migration, and cell cycle progression of human vascular smooth muscle cells in atherosclerosis

Zhang

Chen

et al. 2021

Open Life Sciences

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The circ_UBR4 (hsa_circ_0010283) is a novel abnormally overexpressed circRNA in oxidized low-density lipoprotein (ox-LDL)-induced model of atherosclerosis (AS) in human vascular smooth muscle cells (VSMCs). However, its role in the dysfunction of VSMCs remains to be further investigated. Here, we attempted to explore its role in ox-LDL-induced excessive proliferation and migration in VSMCs by regulating Rho/Rho-associated coiled-coil containing kinase 1 (ROCK1), a therapeutic target of AS. Expression of circ_UBR4 and ROCK1 was upregulated, whereas miR-107 was downregulated in human AS serum and ox-LDL-induced VSMCs. Depletion of circ_UBR4 arrested cell cycle, suppressed cell viability, colony-forming ability, and migration ability, and depressed expression of proliferating cell nuclear antigen and matrix metalloproteinase 2 in VSMCs in spite of the opposite effects of ox-LDL. Notably, ROCK1 upregulation mediated by plasmid transfection or miR-107 deletion could counteract the suppressive role of circ_UBR4 knockdown in ox-LDL-induced VSMCs proliferation, migration, and cell cycle progression. In mechanism, miR-107 was identified as a target of circ_UBR4 to mediate the regulatory effect of circ_UBR4 on ROCK1. circ_UBR4 might be a contributor in human AS partially by regulating VSMCs’ cell proliferation, migration, and cell cycle progression via circ_UBR4/miR-107/ROCK1 pathway.

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“…The miRNA expression change is also correlated with the pathogenesis of multiple cancers such as in the lungs, pancreas, and liver to regulate cancer cells initiation, development, and metastasis [ 39 ]. Previous studies have indicated that miR-107 is a tumor suppressor in many cancers such as lung cancer [ 40 ], melanoma [ 41 ], and oral squamous cell carcinoma [ 42 ]. However, other studies have shown that miR-107 can induce chemoresistance in colon cancer by targeting calcium-related proteins [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

Hsa-miR-107 regulates chemosensitivity and inhibits tumor growth in hepatocellular carcinoma cells

Chen

Lin

et al. 2021

Aging

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Hepatocellular carcinoma is a common type of liver cancer. Resistance to chemotherapeutic agents is a major problem in cancer therapy. MicroRNAs have been reported in cancer development and tumor growth; however, the relationship between chemoresistance and hepatocellular carcinoma needs to be fully investigated. Here, we treated hepatocellular carcinoma cell line (HA22T) with a histone deacetylase inhibitor to establish hepatocellular carcinoma-resistant cells (HDACi-R) and investigated the molecular mechanisms of chemoresistance in HCC cells. Although histone deacetylase inhibitor could not enhance cell death in HDACi-R but upregulation of miR-107 decreased cell viability both in parental cells and resistance cells, decreased the expression of cofilin-1, enhanced ROS-induced cell apoptosis, and dose-dependently sensitized HDACi-R to HDACi. Further, miR-107 upregulation resulted in tumor cell disorganization in both HA22T and HDACi-R in a mice xenograft model. Our findings demonstrated that miR-107 downregulation leads to hepatocellular carcinoma cell resistance in HDACi via a cofilin-1-dependent molecular mechanism and ROS accumulation.

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MicroRNA‑107 may regulate lung cancer cell proliferation and apoptosis by targeting TP53 regulated inhibitor of apoptosis 1

Cited by 8 publications

References 33 publications

PCGEM1 promotes proliferation, migration and invasion in prostate cancer by sponging miR-506 to upregulate TRIAP1

PCGEM1 promotes proliferation, migration and invasion in prostate cancer by sponging miR-506 to upregulate TRIAP1

Blocking circ_UBR4 suppressed proliferation, migration, and cell cycle progression of human vascular smooth muscle cells in atherosclerosis

Hsa-miR-107 regulates chemosensitivity and inhibits tumor growth in hepatocellular carcinoma cells

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