miR-100-3p inhibits cell proliferation and induces apoptosis in human gastric cancer through targeting to BMPR2

Peng, Changhong; Yue, Lingxiao; Zhou, Yuanqin; Tang, Sai Wen; Chen, Kan; Xia, Leiming; Yang, Fan; Wang, Siying

doi:10.1186/s12935-019-1060-2

Cited by 22 publications

(9 citation statements)

References 33 publications

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“…Controversial reports exist about the role of miR‐99 family members in cancer progression. MiR‐99a is often found to be downregulated in GC tissues (Peng et al, 2019). Cao et al (2018) also showed that out of 38 GC tissues, miR‐100 was downregulated in 30 cases and low levels of miR‐100 correlated with poor disease prognosis.…”

Section: Mir‐99 Family Members In Cancersmentioning

confidence: 99%

“…MiR‐99a and miR‐99b were reported to target IGF‐1R and thereby inhibit cell proliferation (Wang, Zhao, et al, 2018; Xu et al, 2019). The tumor suppressor role of miR‐99a can also be achieved via suppression of bone morphogenetic protein receptor 2 (BMPR2) (Peng et al, 2019). The oncogenic lncRNA HAGLROS was also shown to titrate the level of free miR‐100 in GC cells, indicating the role of miR‐100 as a TSmiR (Chen et al, 2018).…”

Section: Mir‐99 Family Members In Cancersmentioning

confidence: 99%

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MicroRNA‐99 family in cancer and immunity

Eniafe

Jiang

2020

WIREs RNA

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The microRNA (miR)‐99 family comprising miR‐99a, miR‐99b, and miR‐100 is an evolutionarily conserved family with existence dating prior to the bilaterians. Members are typically oncogenic in leukemia while their functional roles in other cancers alternate between that of a tumor suppressor and a tumor promoter. Targets of the miR‐99 family rank in the lists of oncogenes and tumor suppressors, thereby illustrating the dual role of this miR family as oncogenic miRs (oncomiRs) and tumor suppressing miRs (TSmiRs) in different cellular contexts. In addition to their functional roles in cancers, miR‐99 family is implicated in the modulation of macrophage inflammatory responses and T‐cell subsets biology, thereby exerting critical roles in the maintenance of tissue homeostasis, establishment of peripheral tolerance as well as resolution of an inflammatory reaction. Here, we review emerging knowledge of this miR family and discuss remaining concerns linked to their activities. A better dissection of the functional roles of miR‐99 family members in cancer and immunity will help in the development of novel miR‐99‐based therapeutics for the treatment of human cancer and immune‐related diseases. This article is categorized under: RNA in Disease and Development > RNA in Disease

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Section: Mir‐99 Family Members In Cancersmentioning

confidence: 99%

Section: Mir‐99 Family Members In Cancersmentioning

confidence: 99%

MicroRNA‐99 family in cancer and immunity

Eniafe

Jiang

2020

WIREs RNA

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“…(G) Proliferation and invasion assays in SW780 cells after overexpression of miR-3127. *P < 0.05. performed as previously reported (Peng et al, 2019). In brief, T24 cells were infected by miR-3127-overexpression lentiviral vector or control vector, and SW780 cells were infected by miR-3127sponge lentiviral vector or control vector.…”

Section: Lentiviral Transfectionmentioning

confidence: 99%

LINC00319-Mediated miR-3127 Repression Enhances Bladder Cancer Progression Through Upregulation of RAP2A

Wang

Meng

2020

Front. Genet.

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Recent studies suggested that microRNA-3127 (miR-3127) was dysregulated in multiple tumor types and has important roles in tumorigenesis and cancer progression. However, its biological roles and the mechanisms that regulate its expression in bladder cancer (BCA) remain to be determined. The expression level of miR-3127 was measured in BCA tissues and its cellular functions were examined using both in vitro and in vivo experiments. The interaction between miR-3127 and long non-coding RNA (lncRNA) LINC00319 was explored using RNA immunoprecipitation assay and luciferase reporter assays. We showed that miR-3127 expression was significantly downregulated in human BCA tissues and BCA cell lines. Lower miR-3127 levels were associated with worse survival in BCA patients. The overexpression of miR-3127 impaired BCA cell proliferation and invasion, and the knockdown of miR-3127 enhanced BCA cell proliferation and invasion in vitro. Importantly, miR-3127 was able to suppress cell growth in vivo. We demonstrated that miR-3127 repressed the proliferation and invasion of BCA cells though directly targeted the 3-UTR of RAP2A, which served as a novel oncogene in BCA cells. The suppression of cell proliferation and invasion caused by miR-3127 overexpression could be partially abrogated by ectopic expression of RAP2A. Furthermore, high expression of LINC00319 was correlated with adverse survival in BCA patients. LINC00319 could bind directly with miR-3127 and inhibited its expression, and the tumor-promoting effects of LINC00319 could be reversed by re-expression of miR-3127 in BCA cells. Our findings indicated that lncRNA LINC00319-mediated miR-3127 repression promotes BCA progression through the upregulation of RAP2A. The re-introduction of miR-3127 or inhibition of LINC00319 might represent a promising therapeutic strategy for BCA treatment.

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“…By comparing the expression levels of miRNAs between 0.5% FBS and 10% FBS in human Sertoli cells, we revealed that miR-100-3p was enhanced by 10% FBS, as demonstrated by miRNA microarray and verified by real-time qPCR. MiR-100-3p has been shown to control the proliferation and the apoptosis of human gastric cancer cells via binding to bone morphogenic protein type 2 receptor (BMPR2) ( Peng et al, 2019 ), and it may be involved in producing interleukin (IL)-8 and IL-1β in mesangial cells ( Liang et al, 2016 ). In this study, we have shown that miR-100-3p stimulates human Sertoli cell proliferation and DNA synthesis, as determined by CCK-8 assay, PCNA expression, and EdU incorporation assay.…”

Section: Discussionmentioning

confidence: 99%

Hsa-miR-100-3p Controls the Proliferation, DNA Synthesis, and Apoptosis of Human Sertoli Cells by Binding to SGK3

Liu

Cui

Chen

et al. 2021

Front. Cell Dev. Biol.

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Human Sertoli cell is required for completing normal spermatogenesis, and significantly, it has important applications in reproduction and regenerative medicine because of its great plasticity. Nevertheless, the molecular mechanisms underlying the fate decisions of human Sertoli cells remain to be clarified. Here, we have demonstrated the expression, function, and mechanism of Homo sapiens-microRNA (hsa-miR)-100-3p in human Sertoli cells. We revealed that miR-100-3p was expressed at a higher level in human Sertoli cells by 10% fetal bovine serum (FBS) than 0.5% FBS. MiR-100-3p mimics enhanced the DNA synthesis and the proliferation of human Sertoli cells, as indicated by 5-ethynyl-2′-deoxyuridine (EdU) and Cell Counting Kit-8 (CCK-8) assays. Flow cytometry showed that miR-100-3p mimics reduced the apoptosis of human Sertoli cells, and notably, we predicted and further identified serum/glucocorticoid regulated kinase family member 3 (SGK3) as a direct target of MiR-100-3p. SGK3 silencing increased the proliferation and decreased the apoptosis of human Sertoli cells, while SGK3 siRNA 3 assumed a similar role to miR-100-3p mimics in human Sertoli cells. Collectively, our study indicates that miR-100-3p regulates the fate decisions of human Sertoli cells by binding to SGK3. This study is of great significance, since it provides the novel epigenetic regulator for the proliferation and apoptosis of human Sertoli cells and it may offer a new clue for gene therapy of male infertility.

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miR-100-3p inhibits cell proliferation and induces apoptosis in human gastric cancer through targeting to BMPR2

Cited by 22 publications

References 33 publications

MicroRNA‐99 family in cancer and immunity

MicroRNA‐99 family in cancer and immunity

LINC00319-Mediated miR-3127 Repression Enhances Bladder Cancer Progression Through Upregulation of RAP2A

Hsa-miR-100-3p Controls the Proliferation, DNA Synthesis, and Apoptosis of Human Sertoli Cells by Binding to SGK3

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