miR-936 Suppresses Cell Proliferation, Invasion, and Drug Resistance of Laryngeal Squamous Cell Carcinoma and Targets GPR78

Lin, Xi-Jun; Liu, Hui; Li, Pei; Wang, Haifeng; Yang, Ankui; Di, Jiejian; Jiang, Qiwei; Yang, Yang; Huang, Jingmin; Yuan, Meng-Ling; Xing, Zihao; Wei, Meng-Ning; Li, Yao; Shi, Zhi

doi:10.3389/fonc.2020.00060

Cited by 32 publications

(31 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent studies have demonstrated that combination treatment with some miRNAs is able to reduce the chemoresistance of cancers. [35][36][37][38] Among these miRNAs, miR-140 is reported to function as a tumor suppressor. [24][25][26] Furthermore, previous studies have indicated that miR-140 can enhance chemosensitivity of some cancers.…”

Section: Discussionmentioning

confidence: 99%

<p>MiR-140 Resensitizes Cisplatin-Resistant NSCLC Cells to Cisplatin Treatment Through the SIRT1/ROS/JNK Pathway</p>

Lin¹,

Pan²,

Chen³

et al. 2020

OTT

View full text Add to dashboard Cite

Background: Although cisplatin is an effective chemotherapeutic drug that is commonly used for non-small-cell lung cancer (NSCLC) treatment, the drug resistance usually occurs during the long-term use of it. It is urgent to develop strategies to reduce the resistance of NSCLC cells to cisplatin. Methods: Cisplatin-resistant NSCLC cell lines (PC9/R and A549/R) were acquired through long-term exposure of PC9 and A549 cells to cisplatin. QRT-PCR analysis was performed to compare the expression of miR-140 between routine NSCLC cells and cisplatin-resistant NSCLC cells. CCK-8 assay was used to evaluate the effect of miR-140 on the sensitivity of PC9/R and A549/R to cisplatin. Western blot assay and luciferase reporter assay were used to confirm the regulation of miR-140 on SIRT1. Western blot and flow cytometry analysis were performed to evaluate the effect of miR-140 on the apoptosis pathway induced by cisplatin. Results: PC9/R and A549/R exhibited obviously lower sensitivity compared to their parental PC9 and A549 cells, respectively. Furthermore, PC9/R and A549/R cells expressed significantly lower levels of miR-140 compared to their parental PC9 and A549 cells, respectively. However, transfection with miR-140 mimics significantly resensitized the PC9/R and A549/R to cisplatin-induced cytotoxicity. In the mechanism research, we confirmed that SIRT1 was overexpressed and was targeted by miR-140 in PC9/R and A549/R. Furthermore, overexpression of SIRT1 was responsible for the resistance to cisplatin in PC9/ R and A549/R cells. Transfection with miR-140 was able to inhibit the expression of SIRT1 and thus inhibited the SIRT1/ROS/JNK pathway. As a result, the PC9/R and A549/R cells restored the sensitivity to cisplatin-induced apoptosis. Conclusion: MiR-140 resensitizes cisplatin-resistant NSCLC cells to cisplatin treatment through the SIRT1/ROS/JNK pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

<p>MiR-140 Resensitizes Cisplatin-Resistant NSCLC Cells to Cisplatin Treatment Through the SIRT1/ROS/JNK Pathway</p>

Lin¹,

Pan²,

Chen³

et al. 2020

OTT

View full text Add to dashboard Cite

show abstract

“…This finding suggested that miR-503-5p may play an unknown role in the effect of tobacco on SCCHN. In general, miRNAs exert diverse regulatory roles through target differential mRNAs [11,14,16,22,40], same for miR-223-3p and miR-204-5p. Considering the potential clinical significance of miR-223-3p and miR-204-5p, it is necessary and worthy to define the possible targets for providing reference for the followed study.…”

Section: Discussionmentioning

confidence: 99%

Clinical significance and potential mechanisms of miR-223-3p and miR-204-5p in squamous cell carcinoma of head and neck: a study based on TCGA and GEO

et al. 2020

View full text Add to dashboard Cite

ObjectiveTo explore the clinical significance and mechanisms of altered miRNAs in squamous cell carcinoma of head and neck (SCCHN) and provide references for SCCHN diagnosis and prognosis.MethodDifferential expressed miRNAs (DEMs) in SCCHN were screened through gene expression omnibus (GEO) DataSets and verified by the cancer genome atlas (TCGA) database. Next, the overall survival analysis, receiver operating characteristics, and clinical correlation analysis were adopted to filter the miRNAs with diagnostic and prognostic values. Finally, functional enrichment analyses were conducted for inquiring into the mechanisms of miRNAs.ResultsTotal 103 DEMs (p < 0.05, fold change ≥ 2) in SCCHN were screened out from GSE124566. Partly, the expression levels of the selected (12/17) miRNAs were verified by TCGA. Followed, of the 12 miRNAs, two miRNA expression levels were associated with the overall survival, and five miRNAs showed diagnostic values (AUC ≥ 0.85). Besides, miR-223-3p and miR-204-5p expression levels were correlated to certain clinical features. Epithelial–mesenchymal transition (EMT) related biological process and energy metabolism controlling related AMPK signaling pathway might mediate the roles of miR-223-3p and miR-204-5p, respectively.ConclusionWith diagnostic and prognostic values, miR-223-3p and miR-204-5p may be involved in the progression of SCCHN through EMT-related biological process and energy balance related AMPK signaling pathway, respectively.

show abstract

“…13 However, the recurrence, metastasis, and insensitivity to radiotherapy or chemoresistance often lead to poor therapeutic effects for LSCC, which cannot be solved by traditional therapies. 14,15 Therefore, it is urgent to identify novel targets for the treatment of LSCC. In the present study, we demonstrated that USP34 promoted LSCC cell survival and drug resistance by stabilizing SOX2, and targeting USP34/SOX2 axis may be a promising strategy to combat LSCC.…”

Section: Discussionmentioning

confidence: 99%

The deubiquitinase USP34 stabilizes SOX2 and induces cell survival and drug resistance in laryngeal squamous cell carcinoma

Dai

Yuan

Cao³

2020

The Kaohsiung J of Med Scie

View full text Add to dashboard Cite

Recent studies showed that the deubiquitinase ubiquitin‐specific protease 34 (USP34) was involved in the tumorigenesis of several tumors, but its function and mechanism are still unclear in laryngeal squamous cell carcinoma (LSCC). In this study, we found that USP34 and SOX2 were elevated in LSCC tumor tissues, and we also found that USP34 expression was positively correlated with SOX2 expression. Our further studies showed that USP34 regulated the protein level of SOX2 in LSCC cells, but not the mRNA level, which suggested that USP34 stabilized SOX2. Moreover, USP34, as a deubiquitinase, could interact with SOX2, and reduce the polyubiquitination of SOX2. In addition, knockdown of USP34 could significantly inhibit LSCC cell growth, but overexpression of SOX2 could reverse this effect. Finally, we also found that USP34 and SOX2 were upregulated in cisplatin‐resistant LSCC cells, but knockdown of USP34 could enhance the drug sensitivity of cisplatin in the resistant cells. Collectively, targeting USP34/SOX2 axis may be a promising strategy for the treatment of LSCC.

show abstract

miR-936 Suppresses Cell Proliferation, Invasion, and Drug Resistance of Laryngeal Squamous Cell Carcinoma and Targets GPR78

Cited by 32 publications

References 26 publications

<p>MiR-140 Resensitizes Cisplatin-Resistant NSCLC Cells to Cisplatin Treatment Through the SIRT1/ROS/JNK Pathway</p>

<p>MiR-140 Resensitizes Cisplatin-Resistant NSCLC Cells to Cisplatin Treatment Through the SIRT1/ROS/JNK Pathway</p>

Clinical significance and potential mechanisms of miR-223-3p and miR-204-5p in squamous cell carcinoma of head and neck: a study based on TCGA and GEO

The deubiquitinase USP34 stabilizes SOX2 and induces cell survival and drug resistance in laryngeal squamous cell carcinoma

Contact Info

Product

Resources

About