Loss of BAX by miR-365 Promotes Cutaneous Squamous Cell Carcinoma Progression by Suppressing Apoptosis

Zhou, Liang; Gao, Rong; Wang, Yinghui; Zhou, Meijuan; Ding, Zhenhua

doi:10.3390/ijms18061157

Cited by 37 publications

(25 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, the expression of RETREG1 was negatively regulated by miR-186 in CSCC cells, and restoration of RETREG1 attenuated the effects of miR-186 on CSCC cells. In recent decades, a large number of miRs, including, miR-125b (11), miR-365 (20), miR-205 (21), miR-199a-5p (22), and miR-203 (23) have been identified as key regulators of the development and progression of CSCC and numerous other types of human cancer. For instance, miR-199a-5p induces CSCC cell invasion by suppressing E-cadherin expression (22).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑186 promotes cell proliferation and inhibits cell apoptosis in cutaneous squamous cell carcinoma by targeting RETREG1

Liu

et al. 2019

Exp Ther Med

View full text Add to dashboard Cite

MicroRNAs (miRs), a class of small non-coding RNAs, have been demonstrated to be involved in the development and progression of human malignancies, including cutaneous squamous cell carcinoma (CSCC). miR-186 serves a suppressive role in certain common types of human cancer; however, its exact function in CSCC has not been reported previously. In the present study, the expression of miR-186 was significantly increased in CSCC tissues compared with adjacent non-tumour tissues. Overexpression of miR-186 significantly promoted CSCC cell proliferation while inhibiting cell apoptosis. Reticulophagy regulator 1 (RETREG1), a gene that is significantly downregulated in CSCC tissues and cell lines, was identified as a novel target of miR-186. In addition, the expression of RETREG1 was inversely correlated with miR-186 expression in CSCC tissues. Furthermore, the expression of RETREG1 was negatively regulated by miR-186 in CSCC cells, and restoration of RETREG1 attenuated the effects of miR-186 on CSCC cells. Taken together, the results of the current study suggest that miR-186 serves an oncogenic role in CSCC and may be used as a potential therapeutic target for the treatment of this disease.

show abstract

Section: Discussionmentioning

confidence: 99%

MicroRNA‑186 promotes cell proliferation and inhibits cell apoptosis in cutaneous squamous cell carcinoma by targeting RETREG1

Liu

et al. 2019

Exp Ther Med

View full text Add to dashboard Cite

show abstract

“…Bcl-2 is generally considered to be an anti-apoptotic protein that serves an important role in promoting cellular survival and inhibiting the actions of pro-apoptotic proteins (29). By contrast, Bax is identified as a pro-apoptotic member of the Bcl-2 protein family that stimulates apoptosis by heterodimerizing with Bcl-2 to inhibit its anti-apoptotic function (30). To date, it has been widely reported that the Bcl-2/Bax ratio is a key factor that reflects the degree of cell apoptosis resistance (31).…”

Section: Discussionmentioning

confidence: 99%

Colony stimulating factor‑1 receptor promotes proliferation, migration and invasion in the human nasopharyngeal carcinoma 6‑10B cell line via the phosphoinositide 3‑kinase/Akt pathway

et al. 2018

View full text Add to dashboard Cite

The present study aimed to investigate the effects of colony-stimulating factor-1 receptor (CSF-1R) on proliferation, migration and invasion in the human nasopharyngeal carcinoma (NPC) 6-10B cell line, and to investigate the possible underlying mechanisms. Using a lentiviral transfection method, a virus carrying the CSF-1R gene was transfected into 6-10B cells. The expression of CSF-1R was then detected by reverse transcription-quantitative polymerase chain reaction and western blot analysis, and was revealed to be markedly enhanced in 6-10B cells. Subsequently, an MTT assay was performed to assess cell proliferative ability, and flow cytometric analysis was utilized to measure the apoptotic rate of the cells. Wound healing and Transwell assays were also performed to observe cell migration and invasion capabilities. Additionally, western blot analysis was used to detect the protein expression of the proliferation and apoptosis signaling factors cyclin D1, B-cell lymphoma 2, Bcl-2-associated X protein, and phosphorylated and total extracellular protein kinase B (Akt/PKB) in 6-10B cells. The results showed that CSF-1R overexpression promoted the proliferation, migration and invasion of the 6-10B cells. The corresponding mechanism may be associated with activation of the phosphoinositide 3-kinase/Akt pathway, which promotes cell survival and proliferation. These results indicated a potential molecular target for the treatment of NPC.

show abstract

“…In recent decades, dysregulation of miRNA expression has been demonstrated to occur during the development and progression of CSCC and other types of human cancer [17][18][19][20][21]. For instance, inhibition of miR-21 could suppress CSCC cell growth and invasion by targeting two tumor suppressors, PDCD4 and PTEN [22].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-125b exerts antitumor functions in cutaneous squamous cell carcinoma by targeting the STAT3 pathway

et al. 2020

View full text Add to dashboard Cite

Background: MicroRNA-125b (miR-125b) is downregulated in human cutaneous squamous cell carcinoma (CSCC). However, its function in CSCC has yet to be extensively explored. Here, we analyze the relationship between signal transducer and activator of transcription 3 (STAT3) and miR-125b in CSCC. Methods: Western blotting and quantitative RT-PCR were used to determine the expression of the miR-125b-STAT3 axis in human CSCC tissues and cell lines. The direct regulatory effect of miR-125b on STAT3 expression was assessed using a luciferase reporter gene assay and RNA immunoprecipitation assay. The MTT assay and flow cytometry were used to determine the role of the miR-125b-STAT3 axis in CSCC cell proliferation and apoptosis. Results: MiR-125b expression levels were significantly lower in CSCC cell lines and tissues than in normal cell lines and tissues. STAT3 was identified as the direct target of miR-125b. Upregulation of miR-125b and downregulation of STAT3 suppressed cell proliferation and promoted cell apoptosis. Cyclin D1 and Bcl2 were identified as the downstream targets of the miR-125-STAT3 axis. Conclusions: Our findings indicate that miR-125b acts as a tumor suppressor in CSCC by targeting the STAT3 pathway. This observation increases our understanding of the molecular mechanisms of CSCC. Therapies aimed at activating miR-125b or inhibiting STAT3 signaling should be explored as potential treatments for CSCC.

show abstract

Loss of BAX by miR-365 Promotes Cutaneous Squamous Cell Carcinoma Progression by Suppressing Apoptosis

Cited by 37 publications

References 31 publications

MicroRNA‑186 promotes cell proliferation and inhibits cell apoptosis in cutaneous squamous cell carcinoma by targeting RETREG1

MicroRNA‑186 promotes cell proliferation and inhibits cell apoptosis in cutaneous squamous cell carcinoma by targeting RETREG1

Colony stimulating factor‑1 receptor promotes proliferation, migration and invasion in the human nasopharyngeal carcinoma 6‑10B cell line via the phosphoinositide 3‑kinase/Akt pathway

MicroRNA-125b exerts antitumor functions in cutaneous squamous cell carcinoma by targeting the STAT3 pathway

Contact Info

Product

Resources

About