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This study was implemented to figure out whether lncRNA HOTAIR/miR‐17‐5p/PTEN axis played a role that was opposite to Shenqifuzheng (SQFZ) injection in regulating the chemosensitivity of gastric cancer cells. The gastric cancer tissues were gathered and four gastric cancer cell lines were prepared, including BGC‐823, MGC‐803, SGC‐7901, and MKN28. Moreover, cisplatin, adriamycin, mitomycin, and 5‐fluoroura were managed as the chemo‐therapeutics, and SQFZ was prepared as a Chinese medicine. Striking distinctions of HOTAIR, miR‐17‐5p, and PTEN expressions were observed between gastric cancer tissues and para‐carcinoma normal tissues (P < 0.05). MKN28 was associated with the highest resistance to cisplatin, adriamycin, mitomycin, and 5‐fluoroura among all the cell types, and SQFZ significantly improved the MKN28 cells’ sensitivity to the drugs (P < 0.05). The over‐expressed HOTAIR and miR‐17‐5p, as well as under‐expressed PTEN tended to significantly facilitate the viability, EMT process and proliferation of MKN28 cells that were subject to treatment of chemo‐therapies (P < 0.05). SQFZ could amplify the effects of si‐HOTAIR, miR‐17‐5p inhibitor, and pcDNA‐PTEN on boosting the chemosensitivity of gastric cancer cells (P < 0.05). In addition, HOTAIR was also found to directly target miR‐17‐5p, and PTEN appeared to be subject to the modification of HOTAIR and miR‐17‐5p in its acting on the viability, proliferation, EMT process, and apoptosis of gastric cancer cells. The HOTAIR/miR‐17‐5p/PTEN axis could be regarded as the potential treatment targets for gastric cancer, and adjuvant therapy of SQFZ injection could assist in further improving the treatment efficacy of chemo‐therapies for gastric cancer.

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.

Background:Glutathione peroxidase 8 (GPX8) has previously been shown to play a role in Keshan disease. In the present study, we explored the prognostic relevance of GPX8 expression in patients with gastric cancer (GC) based upon The Cancer Genome Atlas (TCGA) data. Material/Methods:We assessed the relationship between the expression of GPX8 and clinicopathological findings in GC patients via logistic regression analyses, Kruskal-Wallis tests, and Wilcoxon signed-rank tests. We further assessed the prognostic relevance of specific variables using Kaplan-Meier and Cox regression analyses. We lastly conducted gene set enrichment analyses (GSEA). Results:We detected a significant association between elevated GPX8 levels and more advanced GC tumor stage (OR=5.92 for I vs. IV), as well as more advanced T (OR=22.91 for T1 vs. T4) and N classification (OR=1.82 for N0 vs. N3). We found worse prognosis in patients expressing high levels of GPX8 relative to those with lower expression of this gene (P=0.021). In a univariate analysis, we found high GPX8 expression was strongly correlated with worse OS (hazard ratio [HR]: 1.05; 95% confidence interval [CI]: 1.01 -1.08; P=0.018), and multivariate analysis confirmed that GPX8 expression independently predicts GC patient OS (HR: 1.04; CI: 1.00 -1.08, P=0.041). GSEA revealed that elevated GPX8 expression was associated with enrichment of pathways consistent with MAPK signaling, JAK/STAT signaling, TGF-b signaling, melanoma, and basal cell carcinoma. Conclusions:The expression of GPX8 may have prognostic relevance, being positively associated with worse OS in GC patients.

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