LncRNA-MALAT1 contributes to the cisplatin-resistance of lung cancer by upregulating MRP1 and MDR1 via STAT3 activation

Fang, Zhixian; Chen, Wenyu; Zou, Yuan; Liu, Xinge; Jiang, Hao

doi:10.1016/j.biopha.2018.02.130

Cited by 149 publications

(82 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Furthermore, because we previously demonstrated that MDR1 promotes cabazitaxel resistance of prostate cancer cells, CCL2 and MDR1 are probably directly or indirectly linked to each other. Although there are no studies proving a direct linkage between CCL2 and MDR1, STAT3 activation was shown to induce cisplatin resistance of lung cancer cells via the upregulation of MDR1 . Moreover, the inhibition of STAT3 and AKT, as the upstream of MDR1, was shown to attenuate paclitaxel resistance of lung cancer cells and adriamycin resistance of breast and colon cancer cells .…”

Section: Discussionmentioning

confidence: 99%

“…Although there are no studies proving a direct linkage between CCL2 and MDR1, STAT3 activation was shown to induce cisplatin resistance of lung cancer cells via the upregulation of MDR1. 28 Moreover, the inhibition of STAT3 and AKT, as the upstream of MDR1, was shown to attenuate paclitaxel resistance of lung cancer cells and adriamycin resistance of breast and colon cancer cells. 29 Paclitaxel disrupts the interaction of STAT3 with tubulin, and CCL2 may restore this interaction via activation of STAT3.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

CCL2 induces resistance to the antiproliferative effect of cabazitaxel in prostate cancer cells

et al. 2018

View full text Add to dashboard Cite

Understanding the mechanism of chemoresistance and disease progression in patients with prostate cancer is important for developing novel treatment strategies. In particular, developing resistance to cabazitaxel is a major challenge in patients with docetaxel‐resistant and castration‐resistant prostate cancer (CRPC) because cabazitaxel is often administered as a last resort. However, the mechanism by which cabazitaxel resistance develops is still unclear. C‐C motif chemokine ligands (CCL) were shown to contribute to the castration resistance of prostate cancer cells via an autocrine mechanism. Therefore, we focused on CCL as key factors of chemoresistance in prostate cancer cells. We previously established a cabazitaxel‐resistant cell line, DU145‐TxR/CxR, from a previously established paclitaxel‐resistant cell line, DU145‐TxR. cDNA microarray analysis revealed that the expression of CCL2 was upregulated in both DU145‐TxR and DU145‐TxR/CxR cells compared with DU145 cells. The secreted CCL2 protein level in DU145‐TxR and DU145‐TxR/CxR cells was also higher than in parental DU145 cells. The stimulation of DU145 cells with CCL2 increased the proliferation rate under treatments with cabazitaxel, and a CCR2 (a specific receptor of CCL2) antagonist suppressed the proliferation of DU145‐TxR and DU145‐TxR/CxR cells under treatments of cabazitaxel. The CCL2‐CCR2 axis decreased apoptosis through the inhibition of caspase‐3 and poly(ADP‐ribose) polymerase (PARP). CCL2 is apparently a key contributor to cabazitaxel resistance in prostate cancer cells. Inhibition of the CCL2‐CCR2 axis may be a potential therapeutic strategy against chemoresistant CRPC in combination with cabazitaxel.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

CCL2 induces resistance to the antiproliferative effect of cabazitaxel in prostate cancer cells

et al. 2018

View full text Add to dashboard Cite

show abstract

“…However, due to various reasons, a large number of patients are not sensitive to drugs. Because of complex molecular mechanisms, multiple drug resistance may lead chemotherapeutic failure for lung cancer patients [30].…”

Section: Discussionmentioning

confidence: 99%

LncRNA XIST acts as a microRNA-520 sponge to regulate the cisplatin resistance in NSCLC cells by mediating BAX through ceRNA network

Liu

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: In recent years, LncRNA acts as a member of competing endogenous RNA (ceRNA), playing an important role in drug resistance of lung cancer. The aim of this study was to identify potential biomarkers about cisplatin resistant lung cancer cells using a comprehensive ceRNA network.Methods: GSE6410 (GPL-201) analyzed gene expression changes about cispaltin resistance in A549 NSCLC cells. GSE43249 (GPL-14613) included noncoding RNA expression profiling derived from the cisplatin resistant A549 lung cells. GEO2R, an online analysis tool, analyzed the differentially expressed mRNAs and miRNAs (DEmRNAs and DEmiRNAs). To explore the functional enrichment implication of differentially expressed mRNAs, we used the GO and KEGG pathway analysis. Through miRDB、Targetscan、Starbase、miRWalk, we found targeted miRNAs. The Kaplan-Meier curve method was used to show clinical survival analysis of targeted RNAs (P<0.05). The Starbase database predicted potential lncRNAs mediated targeted miRNAs. Eventually, the novel ceRNA network of lncRNAs, miRNAs, mRNA was constructed by cytoscape3.7.2.Results:118 differentially expressed mRNAs were the basis of the mediated ceRNA network. DAVID and Kaplan-Meier picked out BAX, an apoptosis regulator. Venn Diagram demonstrated 8 miRNAs commomly regulating Bax. Starbase predicted lncRNA XIST mediated miRNAs. Finally, lncRNA XIST maybe a useful biomarker regulating cisplatin resistance in lung cancer cells.Conclusions: LncRNA XIST competitively bound to miRNA 520 in the regulation of cisplatin resistance by BAX , participating apoptosis in the p53 signaling pathway.

show abstract

“…Most of patients have a good initial response to chemotherapy agents, but subsequent relapse is common as largely due to the emergence of drug resistance (Hassan et al 2016). Thus, chemoresistance is consider as one of the main factors of poor prognosis in advanced NSCLC patients (Fang et al 2018). Hence, it's urgently necessary to explore the target and mechanism of chemoresistance in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

Close homologue of L1 sensitizes lung cancer cells to cisplatin and paclitaxel via inhibition Akt pathway

Liu

et al. 2019

Preprint

View full text Add to dashboard Cite

Drug resistance is a serious promble during chemotherapy in lung cancer, which may lead to tumor relapse and further progression. CHL1 was a tumor suppressor in most malignancies, and it was found downregulated in NSCLC cisplatin-resistant cells H460. Thus, in this study, we investigated the role and mechanism of chemoresistance by CHL1 in lung cancer. Human lung adenocarcinoma cell lines A549 and its cisplatin resistant cells (A549/DDP) and paclitaxel resistant cells (A549/PTX) were applied in this research. CHL1 was found obvious downregulation in A549/DDP and A549/PTX cells versus A549 cells. Suppression of CHL1 in A549 cells, promoted cell survival rate and clone formation, decreased cell apoptosis when treated with or without DDP and PTX, respectively. While excessive CHL1 expression in A549/DDP and A549/PTX cells, the results were opposite. Moreover, CHL1 knockdown mediating chemoresistance was reversed by Akt inhibitor SC66 in A549 cells. In summary, overexpression of CHL1 reversed chemoresistance to cisplatin and PTX via suppressing Akt pathway in lung cancer, it was suggested that CHL1 maybe as a potential target for overcome chemoresistance in lung cancer.

show abstract

LncRNA-MALAT1 contributes to the cisplatin-resistance of lung cancer by upregulating MRP1 and MDR1 via STAT3 activation

Cited by 149 publications

References 38 publications

CCL2 induces resistance to the antiproliferative effect of cabazitaxel in prostate cancer cells

CCL2 induces resistance to the antiproliferative effect of cabazitaxel in prostate cancer cells

LncRNA XIST acts as a microRNA-520 sponge to regulate the cisplatin resistance in NSCLC cells by mediating BAX through ceRNA network

Close homologue of L1 sensitizes lung cancer cells to cisplatin and paclitaxel via inhibition Akt pathway

Contact Info

Product

Resources

About