LncRNA HOXA11‐AS drives cisplatin resistance of human LUAD cells via modulating miR‐454‐3p/Stat3

Zhao, Xia; Li, Xiaoyou; Zhou, Leilei; Ni, Jie; Yan, Weigang; Ma, Rong; Wu, Jianzhong; Feng, Jifeng; Chen, Ping

doi:10.1111/cas.13764

Cited by 105 publications

(98 citation statements)

References 26 publications

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“…By contrast, miR-454 inhibited cell proliferation and invasion, but induced apoptosis in gastric cancer (GC) cells by targeting MAPK1 [25], illustrating its tumor suppressive role in GC. Importantly, a more recent study has illustrated that lncRNA HOXA11-AS acts as ceRNA of miR-454 to promote cisplatin resistance in lung adenocarcinoma (LUAD) cells [26]. In the current study, we demonstrate for the first time that miR-454 plays a crucial role in cisplatin resistance in ovarian cancer cells.…”

Section: Discussionsupporting

confidence: 58%

Long Non-coding RNA CCAT1 Sponges miR-454 to Promote Chemoresistance of Ovarian Cancer Cells to Cisplatin by Regulation of Surviving

Wang

Cui

2020

Cancer Res Treat

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PurposeColon cancer-associated transcript 1 (CCAT1) was identified as an oncogenic long non-coding RNA (lncRNA) in a variety of cancers. However, there was a lack of understanding of the mechanism by which CCAT1 conferred cisplatin (also known as DDP) resistance in ovarian cancer cells.Materials and MethodsCell viability of A2780, SKOV3, A2780/DDP, and SKOV3/DDP cells upon cisplatin treatment was monitored by MTT assay. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) detected the expression levels of CCAT1 and miR-454. The effect of sh-CCAT1 on cisplatin response was investigated in xenografts study. Bioinformatic analysis, luciferase reporter assay and qRT-PCR were conducted to validate the direct interaction among CCAT1, miR-454, and survivin. Apoptosis was determined by flow cytometry after dual staining of Annexin-V-FITC/propidium iodide, and the expression of apoptosis-related proteins Bcl-2, Bax and survivin were detected by qRT-PCR and Western blotting. Xenograft study was conducted to monitor in vivo tumor formation.ResultsCCAT1 was highly expressed in cisplatin-resistant ovarian cancer cell line A2780/DDP and SKOV3/DDP. Knockdown of CCAT1 restored sensitivity to cisplatin in vitro and in vivo. Our data revealed that silencing of CCAT1 promoted cisplatin-induced apoptosis via modulating the expression of pro- or anti-apoptotic proteins Bax, Bcl-2, and survivin. CCAT1 directly interacted with miR-454, and miR-454 overexpression potentiated cisplatin-induced apoptosis. Survivin was identified as a functional target of miR-454, restoration of survivin attenuated the effect of miR-454 on cisplatin response. In addition, miR-454 inhibitor or overexpression of survivin was found to abolish sh-CCAT1–induced apoptosis upon cisplatin treatment.ConclusionCCAT1/miR-454/survivin axis conferred cisplatin resistance in ovarian cancer cells.

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Section: Discussionsupporting

confidence: 58%

Long Non-coding RNA CCAT1 Sponges miR-454 to Promote Chemoresistance of Ovarian Cancer Cells to Cisplatin by Regulation of Surviving

Wang

Cui

2020

Cancer Res Treat

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“…Although positive outcomes have been achieved following early diagnosis, the recurrence rate remains unacceptably high, and the 5-year overall survival rate of patients with LUAD remains low (4). Without sufficient early detection methods and effective therapeutic strategies during the early tumor stages, the mortality rate of patients with LUAD has not markedly decreased in recent years (5). Therefore, further insight into the mechanisms responsible for the development and progression of LUAD is urgently required (6).…”

Section: Introductionmentioning

confidence: 99%

Effects of hub genes on the clinicopathological and prognostic features of lung adenocarcinoma

Huang

et al. 2019

Oncol Lett

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Lung adenocarcinoma (LUAD) is a common malignancy; however, the majority of its underlying molecular mechanisms remain unknown. In the present study, weighted gene co-expression network analysis was applied to construct gene co-expression networks for the GSE19804 dataset, in order to screen hub genes associated with the pathogenesis of LUAD. In addition, with the aid of the Database for Annotation, Visualization and Integrated Discovery, Gene Ontology, and Kyoto Encyclopedia of Genes and Genomes, pathway enrichment analyses were performed on the genes in the selected module. Using the GSE40791 dataset and The Cancer Genome Atlas database, the hub genes were identified. It was discovered that the turquoise module was the most significant module associated with the tumor stage of LUAD. After performing functional enrichment analyses, it was indicated that the turquoise module was mainly enriched in signal transduction. Additionally, at the transcriptional and translational level, nine hub genes were identified and validated: Carbonic anhydrase 4 (CA4), platelet and endothelial cell adhesion molecule 1 (PECAM1), DnaJ member B4 (DNAJB4), advanced glycosylation end-product specific receptor (AGER), GTPase, IMAP family member 6 (GIMAP6), chromosome 10 open reading frame 54 (C10orf54), dedicator of cytokinesis 4 (DOCK4), Golgi membrane protein 1 (GOLM1) and platelet activating factor acetylhydrolase 1b catalytic subunit 3 (PAFAH1B3). CA4, PECAM1, DNAJB4, AGER, GIMAP6, C10orf54 and DOCK4 were expressed at lower levels in the tumor samples, whereas GOLM1 and PAFAH1B3 were highly expressed in tumor samples. In addition, all hub genes were associated with prognosis. In conclusion, one module and nine genes were recognized to be associated with the tumor stage of LUAD. These findings may enhance the understanding of the progression and prognosis of LUAD.

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“…microRNA sponge is the main function of lncRNA in tumor chemotherapy. Such as, HOXA11-AS promotes cisplatin resistance of human LUAD cells via sponging miR-454-3p [21]. Linc00518 was demonstrated to decrease chemosensitivity to breast cancer cells through regulating the miR-199a [22] and UCA1 confers PTX resistance to ovarian cancer through silencing miR-129 [23].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA TCL6 enhances preferential toxicity of paclitaxel to renal cell carcinoma cells

Chen¹,

Zhuang²,

Cheng³

et al. 2020

J. Cancer

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Background: Recent findings have shown long non-coding RNAs (lncRNAs) are dysregulated in a variety of cancer cells. In this report, we investigate the effect of T-cell leukemia lymphoma 6 (TCL6) on paclitaxel (PTX)-induced apoptosis in Renal cell carcinoma (RCC) cells. Methods: Expression levels of TCL6 in RCC tissues were analyzed via The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets. Fluorescence in situ hybridization (FISH) was performed to detect the expression of TCL6 in RCC tissues and cells. Two pairs of cell lines were used: TCL6-silenced 786-O cell line and scrambled 786-O cell line, TCL6-overexpressed Caki-1 cell line and Caki-1 scrambled cell line. Cell viability was detected using the MTT assay. Apoptosis was examined by flow cemetery. Dual reporter gene assay was performed to confirm the direct downstream target miRNA of TCL6. Results: Based on RNA sequencing expression data of RCC tissues from TCGA and GEO datasets, the expression deficiency of TCL6 was observed in RCC tissues. Low level of TCL6 was associated with worse overall and disease-free survival of RCC patients. The FISH showed similar results with low expression of TCL6 in RCC tissues and cells. After PTX treatment, a time-dependent decrease in cell viability was observed in TCL6-overexpressed RCC cells and an increase in cell viability was observed in TCL6-silenced cells compared to control cells. Apoptosis induced by PTX was significantly increased in TCL6-overexpressed cells. Inhibition of TCL6 showed a significant decrease in apoptosis. Furthermore, luciferase reporter assay revealed that TCL6 is a direct target gene of miR-221. Conclusions: TCL6 effectively sensitizes RCC to PTX mainly through downregulation of miR-221. Our results suggest that PTX combined with TCL6 might be a potentially more effective chemotherapeutic approach for renal cancer.

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LncRNA HOXA11‐AS drives cisplatin resistance of human LUAD cells via modulating miR‐454‐3p/Stat3

Cited by 105 publications

References 26 publications

Long Non-coding RNA CCAT1 Sponges miR-454 to Promote Chemoresistance of Ovarian Cancer Cells to Cisplatin by Regulation of Surviving

Long Non-coding RNA CCAT1 Sponges miR-454 to Promote Chemoresistance of Ovarian Cancer Cells to Cisplatin by Regulation of Surviving

Effects of hub genes on the clinicopathological and prognostic features of lung adenocarcinoma

Long non-coding RNA TCL6 enhances preferential toxicity of paclitaxel to renal cell carcinoma cells

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