Down‐regulation of miR‐26b induces cisplatin resistance in nasopharyngeal carcinoma by repressing <scp>JAG</scp>1

Shi, Lei; Zhang, Zhe; Shi, Guanggang

doi:10.1002/2211-5463.12135

Cited by 27 publications

(16 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…27,28 Furthermore, previous studies have found that the absence of miR-26b is associated with chemoresistance in cancers, whereas overexpression of miR-26b sensitizes these cancer cells to chemotherapeutic drugs including cisplatin. [29][30][31] In the present study, we demonstrated that miR-26b expression was downregulated in the established cisplatin-resistant NSCLC models. Furthermore, the reduction of miR-26b was associated with the formation of cisplatin resistance in these cisplatin-resistant NSCLC models.…”

Section: Discussionsupporting

confidence: 57%

<p>Restoration of miR-26b expression partially reverses the cisplatin resistance of NSCLC by targeting tafazzin</p>

Zang

Zhao

Gao

et al. 2019

OTT

View full text Add to dashboard Cite

Background: Dysregulation of microRNAs has been reported to be responsible for drug resistance of cancers. However, the association between aberrant expression of miR-26b and cisplatin resistance in non-small cell lung cancer (NSCLC) remains unclear. Methods: PC9 and A549 were used to establish the cisplatin resistance models on NSCLC. Expression of miR-26b in cisplatin-resistant PC9 and A549 cells (PC9/R and A549/R) was detected by quantitative real-time PCR assays. Drug sensitivity and mitochondrial apoptosis were detected by Cell Counting Kit-8 assay and flow cytometry assay, respectively. The target relationship between miR-26b and tafazzin (TAZ) was validated by dual-luciferase reporter assay. Results: Obvious downregulation of miR-26b was observed in PC9/R and A549/R cells. Restoration of miR-26b partially reversed the cisplatin resistance of PC9/R and A549/R cells. Expression of TAZ was increased in PC9/R and A549/R cells compared to the parental PC9 and A549 cells. Results of dual-luciferase reporter assays verified that TAZ was targeted by miR-26b. We showed that restoration of miR-26b expression inhibited the TAZ expression and thus expanded the mitochondrial pathway of apoptosis induced by cisplatin in PC9/ R and A549/R cells. Conclusion: Restoration of miR-26b expression partially reverses the cisplatin resistance of NSCLC by targeting TAZ. miR-26b/TAZ axis may represent a potential strategy to reverse the cisplatin in NSCLC.

show abstract

Section: Discussionsupporting

confidence: 57%

<p>Restoration of miR-26b expression partially reverses the cisplatin resistance of NSCLC by targeting tafazzin</p>

Zang

Zhao

Gao

et al. 2019

OTT

View full text Add to dashboard Cite

show abstract

“…Furthermore, recent studies demonstrate that reduction of miR-26b is responsible for chemoresistance in some cancers such as nasopharyngeal carcinoma, hepatocellular carcinoma and lung cancer. Overexpression of miR-26b sensitizes these cancer cells to cisplatin and doxorubicin [ 31 - 33 ]. These previous reports suggest that miR-26b is a suppressor for chemoresistance.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of miR-26b decreases the cisplatin-resistance in laryngeal cancer by targeting ATF2

et al. 2017

View full text Add to dashboard Cite

Cisplatin is a common used chemotherapeutic drug for the treatment of laryngeal cancer. However, drug-resistance is a major obstacle in platinum-based chemotherapy for laryngeal cancer. Recent studies have demonstrated that dysregulation of microRNAs (miRNAs) is responsible for chemoresistance in multiple cancers including laryngeal cancer, but the potential mechanisms are required to be explored. In the present study, we constantly exposed the laryngeal cancer cell line Hep-2 with cisplatin to establish a cisplatin-resistant laryngeal cancer cell model (Hep-2/R). We found that Hep-2/R cells exhibited obvious resistance to cisplatin compared to the Hep-2 cells. However, overexpression of miR-26b significantly decreased the half maximal inhibitory concentration (IC50) of cisplatin to Hep-2/R. Mechanically, miR-26b in Hep-2/R decreased the expression of ATF2, and thus inhibiting the phosphorylation of ATF2 and formation of cellular ATF2-c-Jun complex induced by cisplatin. As the results, Hep-2/R cells failed to overexpress the Bcl-xl which is a key anti-apoptotic protein under the cisplatin treatment. Therefore, overexpression of miR-26b was found to be able to promote mitochondrial apoptosis induced by cisplatin.

show abstract

“…miRNAs are reported to be novel DDP sensitivity modulators. Recent studies have shown that decreased miR-26b expression could repress JAG1 to induce DDP resistance in NPC (24). As previous research has shown, miR-106a-5p could target FASTK to promote apoptosis associated with the inhibition of proliferation and migration in astrocytoma cells (25).…”

Section: Discussionmentioning

confidence: 87%

HOTAIR Promotes Cisplatin Resistance of Nasopharyngeal Carcinoma Cells by Regulating Cell Proliferation, Invasion, and Apoptosis via miR-106a-5p/SOX4 Axis

Cao

Sun

Liu

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Nasopharyngeal carcinoma (NPC) is a highly malignant neoplasm originating from nasopharyngeal mucosa, and the emergence of multi-drug resistance poses a huge challenge for clinical treatment of NPC. LncRNA HOTAIR (HOX antisense intergenic RNA) has been reported to be associated with many malignancies, including NPC. However, the underlying mechanisms of HOTAIR involved in drug resistance in NPC are obscure.Methods: Quantitative polymerase chain reaction (qPCR) was employed to determine the HOTAIR, miR-106a-5p and SOX4 expression in NPC tissues and cells. The target relationship between HOTAIR and miR-106a-5p or miR-106a-5p and SOX4 was determined using dual-luciferase reporter assay. Cell proliferation, apoptosis, migration and invasion were explored using Cell counting kit-8 (CCK-8), flow cytometer and Transwell assays. The protein levels were confirmed using western blot.Results: Our study showed that HOTAIR was upregulated in cisplatin (DDP)-resistant NPC tissues and cells. HOTAIR knockdown decreased the DDP resistance, drug resistance related gene expression, cell proliferation and invasion, and promoted apoptosis of C666-1/DDP and CNE2/DDP cells. Mechanism researches displayed that miR-106a-5p was down-regulated in DDP-resistant NPC tissues and cells. miR-106a-5p directly bound with HOTAIR and was regulated by HOTAIR. SOX4 was inhibited by miR-106a-5p at a posttranscriptional level, and the transfection of miR-106a-5p reversed the upregulation of SOX4 caused by HOTAIR overexpression. Increase or decrease of miR-106a-5p suppressed the effect of HOTAIR upregulation or downregulation on DDP resistance, cell proliferation, invasion and apoptosis of C666-1/DDP and CNE2/DDP cells. Moreover, the transfection of SOX4 siRNA reversed the decrease of DDP resistance, cell proliferation and invasion, and rescued the increase of apoptosis induced by miR-106a-5p inhibition. Conclusions: These data suggested that HOTAIR enhanced DDP resistance of C666-1/DDP and CNE2/DDP cells by affecting cell proliferation, invasion, and apoptosis via miR-106a-5p/SOX4 axis.

show abstract

Down‐regulation of miR‐26b induces cisplatin resistance in nasopharyngeal carcinoma by repressing JAG1

Cited by 27 publications

References 31 publications

<p>Restoration of miR-26b expression partially reverses the cisplatin resistance of NSCLC by targeting tafazzin</p>

<p>Restoration of miR-26b expression partially reverses the cisplatin resistance of NSCLC by targeting tafazzin</p>

Overexpression of miR-26b decreases the cisplatin-resistance in laryngeal cancer by targeting ATF2

HOTAIR Promotes Cisplatin Resistance of Nasopharyngeal Carcinoma Cells by Regulating Cell Proliferation, Invasion, and Apoptosis via miR-106a-5p/SOX4 Axis

Contact Info

Product

Resources

About