LncRNA SNHG10 suppresses the development of doxorubicin resistance by downregulating miR-302b in triple-negative breast cancer.

Unlike other types of breast cancer, triple negative breast cancer (TNBC) does not respond to therapies targeting human epidermal growth factor receptor-2 (HER2) or hormone therapy, and the prognosis of patients with TNBC is usually poor. The role of long non-coding RNA (lncRNA) small nucleolar RNA host gene 10 (SNHG10) has been investigated in many types of cancer, but its role in TNBC is unknown. This study aimed to explore the role of SNHG10 in TNBC in the context of doxorubicin treatment, a common therapy for TNBC. Analysis of the TCGA dataset revealed the downregulation of SNHG10 in TNBC. The downregulation of SNHG10 of TNBC in TNBC was further confirmed by detecting its expression in 60 patients with TNBC by qPCR. The expression of SNHG10 was further downregulated after doxorubicin treatment. In TNBC, microRNA-302b (miR-302b) was downregulated and was positively correlated with SNHG10. In TNBC cells, overexpression of SNHG10 resulted in upregulation of miR-302b, and methylation-specific PCR analysis showed that SNHG10 negatively regulates the methylation of miR-302b. In addition, doxorubicin treatment resulted in the downregulation of SNHG10 in TNBC cells, and overexpression of SNHG10 and miR-302b promoted apoptosis of doxorubicin-treated TNBC cells. Furthermore, overexpression of both SNHG10 and miR-302b had a stronger effect on apoptosis than that of overexpression of SNHG10 alone. Our study showed that SNHG10 could inhibit the development of resistance to doxorubicin by upregulating miR-302b in TNBC through methylation. Our findings suggested that SNHG10 might serve as a molecular target for intervening in TBNC metastasis.

Results of a randomized and controlled clinical trial evaluating the efficacy and safety of combination therapy with Endostar and S-1 combined with oxaliplatin in advanced gastric cancer.

OBJECTIVES: We aimed to evaluate the efficacy and safety of combination therapy of Endostar (recombinant human endostatin) and S-1 combined with oxaliplatin (SOX) in patients with advanced gastric cancer. METHODS: In this randomized, controlled trial, 165 late-stage gastric cancer patients were assigned to the experimental arm with Endostar in combination with SOX (80 patients) and the control arm with SOX alone (85 patients). The end points of this study included progression-free survival, response rate, and disease-control rate. RESULTS: There was no statistically significant difference in response rate between the experimental arm and the control arm (53.8% vs 42.4%, P=0.188). The difference in disease-control rate was also statistically insignificant between the two arms (85.0% vs 72.9%, P=0.188). Progression-free survival in the experimental arm was significantly higher than that in the control arm (15.0 months vs 12.0 months, P=0.0001). Common adverse events included immunosuppression, gastrointestinal distress, and neuropathy. There was no statistical difference in the incidences of adverse events. CONCLUSION: Combination therapy of Endostar and SOX provides therapeutic benefits to advanced gastric cancer patients, with tolerable adverse effects.