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长链非编码RNA HOTTIP通过调控miR-137表达参与胰腺癌肿瘤细胞的顺铂耐药

LncRNA HOTTIP Participates in Cisplatin Resistance of Tumor Cells by Regulating miR-137 Expression in Pancreatic Cancer.

作者信息

Yin Feng, Zhang Qian, Dong Zhihui, Hu Jie, Ma Zhiqiang

机构信息

Department of Pharmacy, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang 471000, People's Republic of China.

Thyroid and Mammary Surgery, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang 471000, People's Republic of China.

出版信息

Onco Targets Ther. 2020 Apr 1;13:2689-2699. doi: 10.2147/OTT.S234924. eCollection 2020.

DOI:10.2147/OTT.S234924
PMID:32280243
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7132030/
Abstract

AIM

This study aimed to investigate the effect of HOTTIP and miR-137 on cisplatin resistance of pancreatic cancer cells, and study the mechanism of the effect of HOTTIP on the resistance to cisplatin in pancreatic cancer cells, so as to provide new targets for clinical treatment of pancreatic cancer.

METHODS

Pancreatic cancer cells were induced to be resistant to cisplatin by gradually increasing cisplatin concentration at a low concentration gradient in vitro. The changes of HOTTIP and miR-137 were detected, and the effects of HOTTIP and miR-137 on cisplatin efficacy of pancreatic cancer cisplatin-resistant cells were analyzed to explore the mechanism of HOTTIP on cisplatin resistance of pancreatic cancer cells.

RESULTS

After inducing cisplatin resistance in pancreatic cancer cells, the expression level of HOTTIP in pancreatic cancer cells further increased and miR-137 decreased. Silencing HOTTIP or over-expression of miR-137 can increase the sensitivity of pancreatic cancer cisplatin-resistant cells to cisplatin, inhibit the proliferation of pancreatic cancer cells, and promote apoptosis. And we found HOTTIP can target to inhibit miR-137 expression. Rescue experiments showed that regulating miR-137 cannot affect the expression of HOTTIP, miR-137 is a downstream target of HOTTIP, and down-regulation of miR-137 expression can obviously hinder the cisplatin sensitization effect of silencing HOTTIP on cisplatin-resistant pancreatic cancer cells.

CONCLUSION

Silencing HOTTIP reverses cisplatin resistance of pancreatic cancer cells by promoting miR-137 expression.

摘要

目的

本研究旨在探讨HOTTIP和miR-137对胰腺癌细胞顺铂耐药性的影响，研究HOTTIP影响胰腺癌细胞顺铂耐药性的机制，为胰腺癌临床治疗提供新靶点。

方法

体外以低浓度梯度逐步增加顺铂浓度诱导胰腺癌细胞产生顺铂耐药性。检测HOTTIP和miR-137的变化，分析HOTTIP和miR-137对胰腺癌顺铂耐药细胞顺铂疗效的影响，以探究HOTTIP对胰腺癌细胞顺铂耐药性的作用机制。

结果

诱导胰腺癌细胞产生顺铂耐药性后，胰腺癌细胞中HOTTIP表达水平进一步升高，miR-137降低。沉默HOTTIP或过表达miR-137可增加胰腺癌顺铂耐药细胞对顺铂的敏感性，抑制胰腺癌细胞增殖，并促进细胞凋亡。且发现HOTTIP可靶向抑制miR-137表达。挽救实验表明，调控miR-137不影响HOTTIP表达，miR-137是HOTTIP的下游靶点，下调miR-137表达可明显阻碍沉默HOTTIP对顺铂耐药胰腺癌细胞的顺铂增敏作用。

结论

沉默HOTTIP通过促进miR-137表达逆转胰腺癌细胞的顺铂耐药性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43b1/7132030/189486b821c7/OTT-13-2689-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43b1/7132030/93fbe49acfc5/OTT-13-2689-g0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43b1/7132030/bc80a5fa9e6b/OTT-13-2689-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43b1/7132030/2ba8cd745a6a/OTT-13-2689-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43b1/7132030/189486b821c7/OTT-13-2689-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43b1/7132030/93fbe49acfc5/OTT-13-2689-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43b1/7132030/68b0cbc71051/OTT-13-2689-g0002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43b1/7132030/2ba8cd745a6a/OTT-13-2689-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43b1/7132030/189486b821c7/OTT-13-2689-g0007.jpg

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