CCL18-induced HOTAIR upregulation promotes malignant progression in esophageal squamous cell carcinoma through the miR-130a-5p-ZEB1 axis

Wang, Wenjian; Wu, Duoguang; He, Xiaotian; Hu, Xueqiang; Hu, Chuwen; Shen, Zhiwen; Lin, Jiatong; Pan, Zihao; He, Zonglin; Lin, Hongxin; Wang, Minghui

doi:10.1016/j.canlet.2019.06.009

Cited by 53 publications

(42 citation statements)

References 45 publications

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“…We used the GEO database to select mRNAs that were downregulated in SOC, identified potential lncRNA-miRNA-mRNA interaction networks based on the presence of specific binding sites, and reconstructed a comprehensive ceRNA network. Several recent studies demonstrated that ceRNA-based mechanisms may operate in all types of carcinoma [5,6,[17][18][19][20][21][22][23]. In the present study, among the miRNAs found to be downregulated in SOC, hsa-miR-195-5p and hsa-miR-497-5p were predicted to bind to LINC00284.…”

Section: Discussionsupporting

confidence: 54%

Construction and Investigation of an LINC00284-Associated Regulatory Network in Serous Ovarian Carcinoma

et al. 2020

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The low survival rate associated with serous ovarian carcinoma (SOC) is largely due to the lack of relevant molecular markers for early detection and therapy. Increasing experimental evidence has demonstrated that long noncoding RNAs (lncRNAs) are involved in cancer initiation and development, and a competitive endogenous RNA (ceRNA) hypothesis has been formulated. Therefore, the characterization of new lncRNA and lncRNA-related networks is crucial for early diagnosis and targeted therapy of SOC. Data on lncRNAs, mRNAs, and miRNAs with differential expression in SOC, compared to normal ovarian tissue, were obtained from the Gene Expression Omnibus (GEO) database. Data on lncRNA expression and clinical data in SOC were obtained from The Cancer Genome Atlas (TCGA). lncRNA-miRNA interactions were predicted by the miRBase database. Different online tools, i.e., TargetScan, RNA22, miRmap, microT, miRanda, StarBase, and PicTar, were cooperatively utilized to predict the mRNAs targeted by miRNAs. The plugin of BiNGO in Cytoscape and KOBAS 3.0 were used to conduct the functional and pathway enrichment analyses. The lncRNA, miRNAs, and mRNAs identified to be expressed at statistically significant and different levels between SOC and healthy fallopian tube tissues were further validated using qRT-PCR. A total of 4 lncRNAs (LINC00284, HAGLR, HCAT158, and BLACAT1) and 111 mRNAs were found to be upregulated in SOC tissues compared to normal tissues, based on the GEO database. LINC00284 was found to be highly expressed in SOC, in association with the upregulation of the transcription factor SOX9. The high LINC00284 expression was associated with poor prognosis and proved to be an independent risk factor in patients with SOC, based on TCGA database. The qRT-PCR validation results closely recapitulated the expression profiles and prognostic scores of the aforementioned bioinformatic analyses. The LINC00284-related ceRNA network was found to be associated with SOC carcinogenesis by biofunctional analysis. In conclusion, the LINC00284-related ceRNA network may provide valuable information on the mechanisms of SOC initiation and progression. Importantly, LINC00284 proved to be a new potential prognostic biomarker for SOC.

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Section: Discussionsupporting

confidence: 54%

Construction and Investigation of an LINC00284-Associated Regulatory Network in Serous Ovarian Carcinoma

et al. 2020

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“…Esophageal carcinoma is one of the most life-threatening malignancies worldwide (1,2). Esophageal squamous cell carcinoma (EScc) is a major histological type of esophageal carcinoma, and accounts for ~70-80% of esophageal cancer cases in china (3).…”

Section: Introductionmentioning

confidence: 99%

LINC00473 contributes to the radioresistance of esophageal squamous cell carcinoma by regulating microRNA‑497‑5p and cell division cycle 25A

Liu

Qiao

et al. 2020

Int J Mol Med

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Long non-coding RNA (lncRNA) LINc00473 plays a carcinogenic role in a variety of different tumor types. Nevertheless, the mechanisms through which LINc00473 regulates the radiosensitivity of esophageal squamous cell carcinoma (EScc) cells remains elusive. In the present study, reverse transcription-quantitative PcR was used to quantify the expression of LINc00473, microRNA (miRNA/miR)-497-5p and cell division cycle 25A (cdc25A) in EScc tissues. The association between LINc00473 expression and the clinicopathological characteristics of patients with EScc was also assessed. Furthermore, cell counting kit-8 and colony formation assays were carried out to monitor the proliferation of EScc cells exposed to X-ray radiation. A dual-luciferase reporter assay was also conducted to analyze the interaction between LINc00473 and miR-497-5p, as well as the interaction between CDC25A and miR-497-5p. The findings of the present study demonstrated that in EScc tissues and cells, the expression levels of LINC00473 and CDC25A were significantly upregulated, while the expression of miR-497-5p was downregulated. The high expression level of LINc00473 was associated with a higher T stage, lymph node metastasis stage and a lower tumor differentiation grade in patients with EScc. Following irradiation, transfection with miR-497-5p mimics reduced the promoting effect of LINc00473 overexpression on EScc cell proliferation, and partially impeded the resistance of EScc cells to X-ray radiation induced by LINc00473 overexpression. Moreover, transfection with miR-497-5p inhibitors partially alleviated the inhibitory effects of LINc00473 knockdown on cellular proliferation, and partly reversed the sensitivity of cells to X-ray irradiation induced by LINc00473 knockdown. Furthermore, it was confirmed that miR-497-5p was able to bind LINc00473 and the 3'-untranslated region of CDC25A. On the whole, the findings of the present study demonstrate that LINc00473 reduces the radiosensitivity of EScc cells by modulating the miR-497-5p/cdc25A axis.

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“…It can also be regulated by long non-coding RNA HOTAIR and mediate invasion and epithelial-mesenchymal transformation of esophageal squamous cell carcinoma. 25,26 Other studies have verified the influence of miR-130a-5p in GC. For example, Xie et al 27 reported that miR-130a-5p could inhibit the activation of Wnt/β-catenin pathway through targeted inhibition of CB1R, thus exerting tumor resistance and inhibiting malignant progression of GC cells.…”

Section: Discussionmentioning

confidence: 95%

<p>Targeted Inhibition of CCL22 by miR-130a-5p Can Enhance the Sensitivity of Cisplatin-Resistant Gastric Cancer Cells to Chemotherapy</p>

Fang¹,

Li²,

Wang³

et al. 2020

CMAR

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This study set out to explore the regulatory mechanism of miR-130a-5p in cisplatin (DDP)-resistant gastric cancer (GC) cells. Materials and Methods: Forty cases of GC and paracancerous tissues were collected, and the miR-130a-5p and CCL22 levels were detected by qRT-PCR. DDP-resistant cell lines of GC cells were established. Cell viability, invasion, and apoptosis were measured by CCK-8, Transwell, and flow cytometry, respectively. The relationship between miR-130a-5p and CCL22 was verified by dual-luciferase reporter enzyme, and the protein levels of caspase-3, bax, bcl-2, and CCL22 were determined by Western blot. Results: miR-130a-5p was low expressed in GC tissues and cells, while CCL22 showed marked negative correlation, and the area under the curve (AUC) for diagnosing GC was not less than 0.850. Up-regulating miR-130a-5p or knocking down CCL22 expression can inhibit the proliferation and invasion of GC cells and promote their apoptosis, reverse the resistance of NCI-N87/DDP to DDP, and also enhance the chemosensitivity of GC cells. Dualluciferase reporter enzyme identified that there was a targeted relationship between miR-130a-5p and CCL22. At the same time, miR-130a-5p and CCL22 were up-regulated or down-regulated, and the malignant proliferation, invasion, apoptosis, and DDP chemotherapy resistance of the cells had no difference compared with miR-NC with transfectionunrelated sequences. Conclusion: Up-regulating miR-130a-5p can enhance the sensitivity of DDP-resistant GC cells to chemotherapy and regulate their biological function by targeted inhibition of CCL22.

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CCL18-induced HOTAIR upregulation promotes malignant progression in esophageal squamous cell carcinoma through the miR-130a-5p-ZEB1 axis

Cited by 53 publications

References 45 publications

Construction and Investigation of an LINC00284-Associated Regulatory Network in Serous Ovarian Carcinoma

Construction and Investigation of an LINC00284-Associated Regulatory Network in Serous Ovarian Carcinoma

LINC00473 contributes to the radioresistance of esophageal squamous cell carcinoma by regulating microRNA‑497‑5p and cell division cycle 25A

<p>Targeted Inhibition of CCL22 by miR-130a-5p Can Enhance the Sensitivity of Cisplatin-Resistant Gastric Cancer Cells to Chemotherapy</p>

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