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

ABSTRACT: ObjectiveThis study set out to explore the regulatory mechanism of miR-130a-5p in cisplatin (DDP)-resistant gastric cancer (GC) cells.Materials and MethodsForty 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.ResultsmiR-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. Dual-luciferase 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 transfection-unrelated sequences.ConclusionUp-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.

SUBMITTER: Fang Q

PROVIDER: S-EPMC7263884 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Project description:The current investigation explored the synthetic contribution of lncRNA H19, miR-130a-3p, and miR-17-5p to radio-resistance and chemo-sensitivity of cardiac cancer cells. Totally 284 human cardiac cancer tissues were gathered, and they have been pathologically diagnosed. The cardiac cancer cells were isolated with utilization of the mechanic method. Moreover, cisplatin, adriamycin, mitomycin, and 5-fluorouracil were designated as the chemotherapies, and single-dose X-rays were managed as the radiotherapy for cardiac cancer cells. We also performed luciferase reporter gene assay to verify the targeted relationship between H19 and miR-130a-3p, as well as between H19 and miR-17-5p. Finally, mice models were established to examine the functions of H19, miR-130a-3p, and miR-17-5p on the development of cardiac cancer. The study results indicated that H19, miR-130a-3p, and miR-17-5p expressions within cardiac cancer tissues were significantly beyond those within adjacent nontumor tissues (P < 0.05), and H19 expression was positively correlated with both miR-130a-3p (rs = 0.43) and miR-17-5p (rs = 0.49) expressions. The half maximal inhibitory concentrations (IC50) of cisplatin, adriamycin, mitomycin, and 5-fluorouracil for cardiac cancer cells were, respectively, determined as 2.01 μg/mL, 8.35 μg/mL, 24.44 μg/mL, and 166.42 μg/mL. The overexpressed H19, miR-130a-3p, and miR-17-5p appeared to improve the survival rate and viability of cardiac cancer cells that were exposed to chemotherapies and X-rays (all P < 0.05). It was also drawn from luciferase reporter gene assay that H19 could directly target miR-130a-3p and miR-17-5p, thereby modifying the sensitivity of cardiac cancer cells to drugs and X-rays (P < 0.05). Finally, the mice models also produced larger tumor size and higher tumor weight, when H19, miR-130a-3p, or miR-17-5p expressions were up-regulated within them (P < 0.05). In conclusion, H19 could act on miR-130a-3p or miR-17-5p to alter the radio- and chemo-sensitivities of cardiac cancer cells, helping to improve the radio-/chemotherapies for cardiac cancer.

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

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