Overexpression of miR-216b sensitizes NSCLC cells to cisplatin-induced apoptosis by targeting c-Jun

Huang, Gang; Pan, Jiongwei; Ye, Zaiting; Fang, Bingmu; Cheng, Wei; Cao, Zhuo

doi:10.18632/oncotarget.22171

Cited by 25 publications

(20 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In cancer cells, cisplatin or other platinum-based drugs induces DNA damage which is an important apoptosis signal, 34 under the effect of cisplatin-dependent apoptosis signal, mitochondria-mediated intrinsic apoptosis pathway, which represents a collapse of mitochondria and activation of caspase-9 and caspase-3, 35,36 will be triggered. In the mitochondria apoptosis pathway, Bcl-2 and reactive oxygen species (ROS) are important regulators.…”

Section: Discussionmentioning

confidence: 99%

<p>Inhibition of TRIM32 Induced by miR-519d Increases the Sensitivity of Colorectal Cancer Cells to Cisplatin</p>

Su¹,

Wang²,

Wang³

et al. 2020

OTT

View full text Add to dashboard Cite

Background: Colorectal cancer is a leading cause of cancer-related death in the world. Despite cisplatin is a commonly used chemotherapeutic drug for the colorectal cancer treatment, resistance of cancer cells to cisplatin restricts its clinical efficacy. It is important to explore the potential mechanisms and take strategies to sensitize colorectal cancer cells to cisplatin treatment. Methods: Differences of TRIM32 and miR-519d expression between colorectal cancer cells and human normal colon epithelial cells were evaluated by qRT-PCR and Western blot assays. Cytotoxicity of cisplatin against colorectal cancer cells was tested by CCK-8 assay. Generation of reactive oxygen species (ROS), mitochondrial membrane potential and apoptosis was measured by flow cytometry. Dual-luciferase reporter assay was used to validate the association between miR-519d and TRIM32. Results: Significant increase of TRIM32 expression in colorectal cancer tissues and cell lines was observed. TRIM32 negatively regulated the cisplatin sensitivity in colorectal cancer cells. Mechanically, overexpression of TRIM32 was induced by decrease of miR-519d. Exogenous miR-519d can inhibit the expression of TRIM32 and thus promoted the cisplatin-induced apoptosis through the mitochondrial pathway. Conclusion: Overexpression of TRIM32 was induced by the absence of miR-519d in colorectal cancer. MiR-519d can be used as a sensitizer during the cisplatin-based chemotherapy of colorectal cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

<p>Inhibition of TRIM32 Induced by miR-519d Increases the Sensitivity of Colorectal Cancer Cells to Cisplatin</p>

Su¹,

Wang²,

Wang³

et al. 2020

OTT

View full text Add to dashboard Cite

show abstract

“…Another study showed that miR 647 overexpression led to decreased migration and invasion of SGC 7901/VCR cells (vincristine-resistant gastric cancer cells) by targeting ankyrin-B (ANK2), focal adhesion kinase (FAK), matrix metalloproteinase (MMP2 and MMP12), cluster of differentiation (CD44), and snail family transcriptional repressor 1 (SNAIL1) [ 21 ]. In addition, overexpression of miR-216b sensitizes non-small cell lung cancer cells to cisplatin-induced apoptosis by targeting c-Jun [ 22 ]. Restoring miR-27b levels was reported to enhance response to paclitaxel by directly targeting casitas B cell lymphoma-b and growth factor receptor-bound protein 2 in breast cancer [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

Hsa-miRNA-143-3p Reverses Multidrug Resistance of Triple-Negative Breast Cancer by Inhibiting the Expression of Its Target Protein Cytokine-Induced Apoptosis Inhibitor 1In Vivo

Deng

Hao

et al. 2018

J Breast Cancer

View full text Add to dashboard Cite

PurposeMultidrug resistance (MDR) remains a major obstacle in the treatment of triple-negative breast cancer (TNBC) with conventional chemotherapeutic agents. A previous study demonstrated that hsa-miRNA-143-3p plays a vital role in drug resistance of TNBC. Downregulation of hsa-miRNA-143-3p upregulated the expression of its target protein cytokine-induced apoptosis inhibitor 1 (CIAPIN1) in order to activate MDR, while upregulation of hsa-miRNA-143-3p effectively enhances the sensitivity of drug-resistant TNBC cells to chemotherapeutics. The present study aimed to further verify these findings in vivo.MethodsWe established a hypodermic tumor nude mice model using paclitaxel-resistant TNBC cells. We expressed ectopic hsa-miRNA-143-3p under the control of a breast cancer-specific human mammaglobin promoter that guided the efficient expression of exogenous hsa-miRNA-143-3p only in breast cancer cells. Thereafter, we overexpressed hsa-miRNA-143-3p in xenografts using a recombinant virus system and quantified the expression of hsa-miRNA-143-3p, CIAPIN1 protein, and proteins encoded by related functional genes by western blot.ResultsWe successfully completed the prospective exploration of the intravenous virus injection pattern from extensive expression to targeted expression. The overexpression of hsa-miRNA-143-3p significantly alleviated chemoresistance of TNBC by inhibiting viability. In addition, we observed that the expression of CIAPIN1 as a hsa-miRNA-143-3p target protein was remarkably decreased.ConclusionWe partly illustrated the mechanism underlying the hsa-miRNA-143-3p/CIAPIN1 drug resistance pathway. HsamiRNA-143-3p as a tumor suppressive microRNA may be a novel target to effectively reverse MDR of TNBC in vivo.

show abstract

“…Recently, scientists have demonstrated that microRNAs modulate drug resistance in various cancers, including NSCLC . Overexpression of miR‐216b can sensitize NSCLC cells to cisplatin‐induced apoptosis by inhibiting c‐Jun . miR‐181c contributes to cisplatin resistance in NSCLC by targeting Wnt inhibition factor 1 .…”

Section: Introductionmentioning

confidence: 99%

“…[11][12][13] Overexpression of miR-216b can sensitize NSCLC cells to cisplatin-induced apoptosis by inhibiting c-Jun. 14 miR-181c contributes to cisplatin resistance in NSCLC by targeting Wnt inhibition factor 1. 15 In addition, miR-30a-5p can increase paclitaxel sensitivity in NSCLC through targeting BCL-2.…”

mentioning

confidence: 99%

EGCG inhibits CSC‐like properties through targeting miR‐485/CD44 axis in A549‐cisplatin resistant cells

Jiang

Chen

et al. 2018

Molecular Carcinogenesis

View full text Add to dashboard Cite

Non-small cell lung cancer (NSCLC) remains one of the most aggressive tumors with low life expectancy worldwide. The existence of cancer stem cells (CSCs) contributes to the failure of cancer treatment resulted from drug resistance. Altered microRNA expression has been observed in human tumors due to its role in tumor growth, progression, and metastasis. Hence, the aim of our present study was to investigate the effects of miR-485 on the CSC-like traits in NSCLC A549-cisplatin resistant cells and concentrate on the underlying molecular mechanism. It was found that CSC-like phenotypes were much more enriched in A549/cisplatin (A549/CDDP) cells compared to A549-parental cells. In addition, we observed that miR-485 was greatly decreased in A549/CDDP cells and miR-485 overexpression was able to decrease the stemness of A549/DDP cells. Meanwhile, epigallocatechin-3-gallate (EGCG), a green tea polyphenol which has been identified as an effective anticancer compound was able to increase miR-485 expression dose-dependently in A549/CDDP cells. Inhibitors of miR-485 remarkably increased CSC-like phenotypes, which could be reversed by indicated doses of EGCG. Moreover, CD44 was predicted as downstream target of miR-485 and the correlation between them was validated by performing dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Subsequently, in vivo experiments were employed to confirm that EGCG restrained CSC-like characteristics by increasing miR-485 and decreasing CD44 expression. Taken together, it was implied that stemness features and CSC population were suppressed by EGCG-modulated miR-485/CD44 axis in A549/CDDP cells.

show abstract

Overexpression of miR-216b sensitizes NSCLC cells to cisplatin-induced apoptosis by targeting c-Jun

Cited by 25 publications

References 39 publications

<p>Inhibition of TRIM32 Induced by miR-519d Increases the Sensitivity of Colorectal Cancer Cells to Cisplatin</p>

<p>Inhibition of TRIM32 Induced by miR-519d Increases the Sensitivity of Colorectal Cancer Cells to Cisplatin</p>

Hsa-miRNA-143-3p Reverses Multidrug Resistance of Triple-Negative Breast Cancer by Inhibiting the Expression of Its Target Protein Cytokine-Induced Apoptosis Inhibitor 1In Vivo

EGCG inhibits CSC‐like properties through targeting miR‐485/CD44 axis in A549‐cisplatin resistant cells

Contact Info

Product

Resources

About