Therapeutic Role of MiR-140-5p for the Treatment of Non-small Cell Lung Cancer

Flamini, Valentina; Jiang, Wen Guo; Cui, Yuxin

doi:10.21873/anticanres.11825

Cited by 24 publications

(21 citation statements)

References 7 publications

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“…It acts by inhibiting the anti-apoptotic Ras signaling cascade (249). Recent studies confirmed also that the loss of regulation of ncRNAs is involved in chemoresistant acquisition (250, 251). The GAS5 lncRNA is implicated in chemoresistance modulation of several different drugs included into this subnetwork (179–182).…”

Section: Drugs/non-coding Rnas Subnetworkmentioning

confidence: 76%

The Network of Non-coding RNAs in Cancer Drug Resistance

et al. 2018

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Non-coding RNAs (ncRNAs) have been implicated in most cellular functions. The disruption of their function through somatic mutations, genomic imprinting, transcriptional and post-transcriptional regulation, plays an ever-increasing role in cancer development. ncRNAs, including notorious microRNAs, have been thus proposed to function as tumor suppressors or oncogenes, often in a context-dependent fashion. In parallel, ncRNAs with altered expression in cancer have been reported to exert a key role in determining drug sensitivity or restoring drug responsiveness in resistant cells. Acquisition of resistance to anti-cancer drugs is a major hindrance to effective chemotherapy and is one of the most important causes of relapse and mortality in cancer patients. For these reasons, non-coding RNAs have become recent focuses as prognostic agents and modifiers of chemo-sensitivity. This review starts with a brief outline of the role of most studied non-coding RNAs in cancer and then highlights the modulation of cancer drug resistance via known ncRNAs based mechanisms. We identified from literature 388 ncRNA-drugs interactions and analyzed them using an unsupervised approach. Essentially, we performed a network analysis of the non-coding RNAs with direct relations with cancer drugs. Within such a machine-learning framework we detected the most representative ncRNAs-drug associations and groups. We finally discussed the higher integration of the drug-ncRNA clusters with the goal of disentangling effectors from downstream effects and further clarify the involvement of ncRNAs in the cellular mechanisms underlying resistance to cancer treatments.

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Section: Drugs/non-coding Rnas Subnetworkmentioning

confidence: 76%

The Network of Non-coding RNAs in Cancer Drug Resistance

et al. 2018

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“…[24][25][26] Furthermore, previous studies have indicated that miR-140 can enhance chemosensitivity of some cancers. [27][28][29] Given this, we studied the potential role of miR-140 in reversing the cisplatin resistance of NSCLC. In the present study, we proved that our established cisplatin-resistant NSCLC cells showed significant resistance to cisplatin treatment.…”

Section: Discussionmentioning

confidence: 99%

“…[24][25][26] Furthermore, previous studies have indicated that miR-140 can enhance chemosensitivity of some cancers including NSCLC. [27][28][29] On the other hand, patients may benefit from miR-140, because miR-140 can attenuate the acute kidney injury induced by cisplatin through the Nrf2/ARE pathway. 30 Here, we investigated the effect of miR-140 on reducing the cisplatin-resistance of NSCLC and then explored the potential mechanisms.…”

Section: Introductionmentioning

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

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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.

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“…Low levels of miRNA-140 correlated with increased sensitivity to etoposide and topotecan in cell lines [155]. Although it has been proposed that it may serve as a tumor suppressive role via VEGF, forced overexpression of miRNA-140-5p in NSCLC cells reduced migration suggesting enhanced sensitivity to gefitinib, DMH1, and cisplatin [156]. Further studies will clarify the role of miR-140-5p in the response of NSCLC to treatment.…”

Section: Mirna-140 Levels Correlate To Chemosensitivity Of Nsclcmentioning

confidence: 96%

MiRNAs as Novel Adipokines: Obesity-Related Circulating MiRNAs Influence Chemosensitivity in Cancer Patients

Withers

Dewhurst

Hammond

et al. 2020

ncRNA

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Adipose tissue is an endocrine organ, capable of regulating distant physiological processes in other tissues via the release of adipokines into the bloodstream. Recently, circulating adipose-derived microRNAs (miRNAs) have been proposed as a novel class of adipokine, due to their capacity to regulate gene expression in tissues other than fat. Circulating levels of adipokines are known to be altered in obese individuals compared with typical weight individuals and are linked to poorer health outcomes. For example, obese individuals are known to be more prone to the development of some cancers, and less likely to achieve event-free survival following chemotherapy. The purpose of this review was twofold; first to identify circulating miRNAs which are reproducibly altered in obesity, and secondly to identify mechanisms by which these obesity-linked miRNAs might influence the sensitivity of tumors to treatment. We identified 8 candidate circulating miRNAs with altered levels in obese individuals (6 increased, 2 decreased). A second literature review was then performed to investigate if these candidates might have a role in mediating resistance to cancer treatment. All of the circulating miRNAs identified were capable of mediating responses to cancer treatment at the cellular level, and so this review provides novel insights which can be used by future studies which aim to improve obese patient outcomes.

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Therapeutic Role of MiR-140-5p for the Treatment of Non-small Cell Lung Cancer

Cited by 24 publications

References 7 publications

The Network of Non-coding RNAs in Cancer Drug Resistance

The Network of Non-coding RNAs in Cancer Drug Resistance

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

MiRNAs as Novel Adipokines: Obesity-Related Circulating MiRNAs Influence Chemosensitivity in Cancer Patients

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