miR-324-5p upregulation potentiates resistance to cisplatin by targeting FBXO11 signalling in non-small cell lung cancer cells

Ba, Zhichang; Zhou, Yufei; Yang, Zhaoyang; Xu, Jianyu; Zhang, Xiu-Shi

doi:10.1093/jb/mvz066

Cited by 17 publications

(21 citation statements)

References 28 publications

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“…FBXO11, a key regulator of EMT, was a verified target of miR-324-5p in lung cancer cells. 22 Consistent with the regulatory association between GATA6-AS1 and miR-324-5p, GATA6-AS1 overexpression elevated FBXO11 protein expression in NCI-H1975 cells ( Figure 5A). As acknowledged, FBXO11 facilitated ubiquitin-mediated degradation of SNAIL protein.…”

Section: Gata6-as1 Promoted Fbxo11 Expressionsupporting

confidence: 77%

“…One recent study discovered that miR-324-5p directly suppressed FBXO11 expression in lung cancer cells. 22 FBXO11 was a member of F-box protein and constituted ubiquitin-protein ligase complex, promoted ubiquitinmediated degradation of SNAIL, a key regulator of EMT, in cancer cells. 24 We experimentally showed that GATA6-AS1 upregulated FBXO11 and downregulated SNAIL protein expression.…”

Section: Discussionmentioning

confidence: 99%

“…Many miRNAs are pivotal for lung cancer development. 19,20 For example, miR-324-5p, which is a recently defined oncogenic miRNA in lung cancer, 21,22 is frequently upregulated in lung cancer and facilitates lung cancer cell proliferation and invasion. 21 In addition, miR-324-5p also targets FBXO11, a regulator of epithelialmesenchymal transition (EMT), to promote development of drug resistance for lung cancer, 22 whereasthe mechanism underlying the aberrant expression of miR-324-5p in lung cancer remains elusive.…”

Section: Introductionmentioning

confidence: 99%

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Long Non-Coding RNA GATA6-AS1 Sponges miR-324-5p to Inhibit Lung Cancer Cell Proliferation and Invasion

Wang

Pan

Yang

et al. 2020

OTT

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Background: Long non-coding RNAs (lncRNAs), which are key regulators of gene expression, are involved in lung cancer progression. Although numerous differentially expressed lncRNAs have been reported, merely a limited number of studies have been performed to verify their functions in lung cancer. Methods: RNA sequencing data were re-analyzed to investigate the GATA6-AS1 expression in lung cancer. RT-qPCR was performed to verify the expression of GATA6-AS1 in collected tissue samples and cell lines. CCK-8 and transwell assays were carried out to evaluate the role of GATA6-AS1 in lung cancer cells. Dual-luciferase reporter assay and bioinformatic analysis were used to explore the miRNA which can be sponged by GATA6-AS1 in lung cancer cells. Results: Currently, we focused on exploring the role and mechanisms of GATA6-AS1 in lung cancer. Expression of GATA6-AS1 was decreased in lung cancer based on the analysis of RNA sequencing dataset, TCGA data and RT-qPCR of clinical tissue samples. Via overexpression of GATA6-AS1, it was revealed that GATA6-AS1 inhibited lung cancer cell proliferation and invasion. Oncogene miR-324-5p was predicted to interact with GATA6-AS1. RT-qPCR and dual-luciferase reporter assay verified the regulation of miR-324-5p by GATG6-AS1 in lung cancer cells. Overexpression of GATA6-AS1 increased the expression of FBXO11 and SP1, two target genes of miR-324-5p. We further showed that miR-324-5p mimic reversed the effect of GATA6-AS1 overexpression in lung cancer cells. Conclusion: Overall, our findings demonstrated GATA6-AS1 as a novel tumor suppressor in lung cancer.

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Section: Gata6-as1 Promoted Fbxo11 Expressionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Long Non-Coding RNA GATA6-AS1 Sponges miR-324-5p to Inhibit Lung Cancer Cell Proliferation and Invasion

Wang

Pan

Yang

et al. 2020

OTT

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“…For example, miR-103a-3p was revealed to potentiate chemoresistance to cisplatin in NSCLC by targeting neurofibromatosis 1, 41 and miR-324-5p contributed to cisplatin resistance in NSCLC by targeting FBXO11 signalling. 42 Previous studies also identified the involvement of miR-608 and miR-328 in the development of cisplatin resistance in NSCLC. 43,44 Furthermore, some circular RNAs, such as hsa_circ_0085131, circ_0076305 and hsa_circ_0001946, have been linked with the resistance to cisplatin in NSCLC.…”

Section: Discussionmentioning

confidence: 98%

LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma

Wang¹,

Gao²,

Chen³

et al. 2020

OTT

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Background: Long non-coding RNAs (lncRNAs) have been found to contribute to cisplatin resistance in several cancers; however, the role of lncRNA LINC01116 in cisplatin resistance remains unknown in non-small-cell lung cancer. This study aimed to examine the contribution of LINC01116 to cisplatin resistance in lung adenocarcinoma (LAD). Materials and Methods: Cisplatin-resistant A549/DDP cells were generated by treatment with cisplatin by dose escalation. LINC01116 expression was compared between A549 and A549/DDP cells, and between cisplatin-resistant and non-resistant LAD specimens. The cell viability, colony formation, proliferation, migration and invasion were measured using MTT and Transwell assays, and cell apoptosis and cell cycle were detected using flow cytometry. The expression of E-cadherin and Vimentin was quantified. LAD xenografts were modeled in nude mice to investigate the role of LINC01116 on the resistance of LAD to cisplatin. Results: MTT assay measured the IC 50 values of 13.49 ± 1.62 and 3.52 ± 1.33 μg/mL for A549/DDP and A549 cells, respectively. LINC01116 was overexpressed in cisplatin-resistant LAD specimens and A549/DDP cells (P < 0.05). Knockdown of LINC01116 inhibited cell viability, proliferation, migration and invasion, promoted apoptosis and enhanced the sensitivity to cisplatin in A549/DDP cells, while LINC01116 overexpression promoted cell viability, proliferation, migration and invasion, inhibited apoptosis and reduced the sensitivity to cisplatin in A549 cells. LINC01116 knockdown resulted in a 2.1-fold increase in E-cadherin expression and a 56% reduction in Vimentin expression in A549/DDP cells, and LINC01116 overexpression resulted in a 45% reduction in E-cadherin expression and a 1.82fold increase in Vimentin expression in A549 cells. Conclusion: Dysregulation of lncRNA LINC01116 expression results in resistance of LAD to cisplatin via the EMT process. Our findings support the oncogenic role of LINC01116 to promote the development of cisplatin resistance in LAD, and LINC01116 may be a novel predictor of poor response to cisplatin.

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“…Collectively, miR-324-5p acted as a tumor suppressor in mountainous cancers, including CRC. Moreover, miR-324-5p was tightly associated with cisplatin resistance in non-small cell lung cancer cells [33]. Hence, we explored whether miR-324-3p could participate in the resistant response in CRC.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA MALAT1 regulates oxaliplatin-resistance via miR-324-3p/ADAM17 axis in colorectal cancer cells

Fan¹,

Yuan²,

Liu³

et al. 2020

Cancer Cell Int

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Background Colorectal cancer (CRC) is one of the most general malignant tumors. Accumulating evidence implied that long non-coding RNA Metastasis Associated Lung Adenocarcinoma Transcript 1 (MALAT1) participated in the tumorigenesis of CRC. However, the effect of MALAT1 in drug-resistance needed to be further illustrated. Methods Levels of MALAT1, microRNA (miR)-324-3p, and a disintegrin and metalloprotease metallopeptidase domain 17 (ADAM17) were detected using quantitative real-time polymerase chain reaction (qRT-PCR) or western blot assay. Cell Counting Kit 8 (CCK-8) was used to assess the half maximal inhibitory concentration (IC50) of oxaliplatin (Ox). Meanwhile, cell proliferation, migration and apoptosis were detected by CCK-8, transwell assay, and flow cytometry, respectively. The interaction between miR-324-3p and MALAT1 or ADAM17 was clarified by dual-luciferase reporter assay. Also, the effect of MALAT1 on tumor growth was detected in xenograft tumor mice treated with Ox. Results Significant up regulation of MALAT1 and ADAM17, and decrease of miR-324-3p were observed in Ox-resistant CRC tissues and cells. MALAT1 deficiency enhanced the sensitivity of Ox-resistant CRC cells response to Ox, while miR-324-3p repression or ADAM17 acceleration could overturn this effect. Moreover, MALAT1 silencing repressed tumor growth in Ox-treated nude mice. Mechanically, MALAT1 exerted promotion effect on the resistance response to Ox via miR-324-3p/ADAM17 axis in Ox-resistant CRC cells. Conclusion MALAT1 modulated the sensitivity of Ox through ADAM17 in Ox-resistant CRC cells by sponging miR-324-3p, thus MALAT1 might serve as a novel insight for the therapy of CRC.

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miR-324-5p upregulation potentiates resistance to cisplatin by targeting FBXO11 signalling in non-small cell lung cancer cells

Cited by 17 publications

References 28 publications

<p>Long Non-Coding RNA GATA6-AS1 Sponges miR-324-5p to Inhibit Lung Cancer Cell Proliferation and Invasion</p>

<p>Long Non-Coding RNA GATA6-AS1 Sponges miR-324-5p to Inhibit Lung Cancer Cell Proliferation and Invasion</p>

<p>LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma</p>

Long non-coding RNA MALAT1 regulates oxaliplatin-resistance via miR-324-3p/ADAM17 axis in colorectal cancer cells

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