A Systematic Review and Meta-Analysis of Comparison of Outcomes of Robot-Assisted versus Open Partial Nephrectomy in Clinical T1 Renal Cell Carcinoma Patients.

INTRODUCTION: Robot-assisted partial nephrectomy (RAPN) has been increasingly used for renal cell carcinoma in recent years. But the advantages of RARN over open partial nephrectomy (OPN) are still controversial. METHODS: We searched the articles between 1997 and 2021 in PubMed, Web of Science, Cochrane Library, and EMbase databases. The parameters were perioperative outcomes including operating time (OT), warm ischemic time (WIT), estimated blood loss (EBL), positive surgical margin (PSM), preoperative and postoperative estimated glomerular filtration rate (eGFR), length of stay (LOS), and intraoperative and postoperative complications. Stata 13.0 software was used for the meta-analysis. RESULTS: Seven studies with 2,646 patients (1,285 in RAPN vs. 1,361 in OPN) were included in the analysis. There were no significant differences in OT (WMD [95% confidence interval (CI)]: 0.14 [-0.33, 0.61], p = 0.570); WIT (WMD [95% CI]:0.28 [-0.13, 0.69], p = 0.187); PSM (odds ratio [OR] [95% CI]: 1.04 [0.37, 2.94], p = 0.944); preoperative eGFR (OR [95% CI]: 0.11 [-0.01, 0.23], p = 0.071); postoperative eGFR (OR [95% CI]: -0.11 [0.27, 0.04], p = 0.159); and intraoperative complications (OR [95% CI]: 0.13 [0.02, 1.04], p = 0.055) between 2 groups. But there were still less EBL (WMD [95% CI]: -0.67 [-1.07, -0.28], p = 0.001), shorter LOS (WMD [95% CI]: -1.09 [-1.86, -0.32], p = 0.005) and fewer postoperative complications (OR [95% CI]: 0.51 [0.38, 0.68], p = 0.000). CONCLUSIONS: Compared with OPN, RAPN appears to achieve partly similar short-term functional outcomes. Meanwhile, some results are inconsistent with previous studies which seem to show that tumor type is also an important factor in comparison between RAPN and OPN, but the analysis is not carried out due to lack of complete data. Therefore, more high-quality random controlled trials are acquired.

Cisplatin resistance in gastric cancer cells is involved with GPR30-mediated epithelial-mesenchymal transition.

Cisplatin is the major chemotherapeutic drug in gastric cancer, particularly in treating advanced gastric cancer. Tumour cells often develop resistance to chemotherapeutic drugs, which seriously affects the efficacy of chemotherapy. GPR30 is a novel oestrogen receptor that is involved in the invasion, metastasis and drug resistance of many tumours. Targeting GPR30 has been shown to increase the drug sensitivity of breast cancer cells. However, few studies have investigated the role of GPR30 in gastric cancer. Epithelial-mesenchymal transition (EMT) has been shown to be associated with the development of chemotherapeutic drug resistance. In this study, we demonstrated that GPR30 is involved in cisplatin resistance by promoting EMT in gastric cancer. GPR30 knockdown resulted in increased sensitivity of different gastric cancer (GC) cells to cisplatin and alterations in the epithelial/mesenchymal markers. Furthermore, G15 significantly enhanced the cisplatin sensitivity of GC cells while G1 inhibited this phenomenon. In addition, EMT occurred when AGS and BGC-823 were treated with cisplatin. Down-regulation of GPR30 with G15 inhibited this transformation, while G1 promoted it. Taken together, these results revealed the role of GPR30 in the formation of cisplatin resistance, suggesting that targeting GPR30 signalling may be a potential strategy for improving the efficacy of chemotherapy in gastric cancer.

Huaier n-butanol extract suppresses proliferation and metastasis of gastric cancer via c-Myc-Bmi1 axis.

Gastric cancer (GC) ranks as the third leading cause of cancer-related mortality worldwide, and approximately 42% of all cases diagnosed each year worldwide are diagnosed in China. A large number of clinical applications have revealed that Trametes robiniophila Μurr. (Huaier) exhibits an anti-tumour effect. However, loss of the bioactive components of Huaier during the extraction procedure with water is unavoidable, and the underlying mechanism of the anti-cancer effect of Huaier remains poorly understood. In this study, we investigated the anti-cancer effect of Huaier n-butanol extract, which contained 51.4% total flavonoids, on HGC27, MGC803, and AGS human GC cell lines in vitro. At a low concentration, Huaier n-butanol extract inhibited the growth of these GC cell types, induced cell cycle arrest and reduced cell metastasis. Moreover, Huaier n-butanol extract suppressed the c-Myc-Bmi1 signalling pathway, and overexpression of Bmi1 reversed the effects of Huaier n-butanol extract on GC cells. Thus, our findings indicate that Huaier n-butanol extract suppresses the proliferation and metastasis of GC cells via a c-Myc-Bmi1-mediated approach, providing a new perspective for our understanding of the anti-tumour effects of Huaier. These results suggest that Huaier n-butanol extract could be an attractive therapeutic adjuvant for the treatment of human GC.

eIF5A2 regulates the resistance of gastric cancer cells to cisplatin via induction of EMT.

Cisplatin is the first-line chemotherapy drug for gastric cancer (GC), but treatment failure often occurs due to development of resistance. The mechanism of cisplatin resistance remains a mystery. Eukaryotic translation initiation factor 5A2 (eIF5A2) is an important tumor-promoting factor and has been rarely studied in GC. This study aimed to investigate the role of eIF5A2 in cisplatin resistance of GC cells and its relationship with epithelial-mesenchymal transition (EMT). We found that it is negative correlation between cisplatin resistance and eIF5A2's expression in GC cells. Silencing of eIF5A2 enhanced the sensitivity of GC cells to cisplatin, while overexpression of eIF5A2 decreased sensitivity. Cisplatin treatment induced gene expression changes consistent with EMT. EMT was blocked and the sensitivity of GC cells to cisplatin was increased by inhibiting the expression of Twist, indicating that EMT regulates the sensitivity of GC cells to cisplatin. Knockdown of eIF5A2 was associated with upregulation of the epithelial markers E-cadherin and ß-catenin, while the expression of mesenchymal markers vimentin and N-cadherin decreased, indicating that eIF5A2 can reverse the EMT process and block the effect of cisplatin on EMT-related markers. Knockdown or overexpression of eIF5A2 did not affect the sensitivity of gastric cancer cells to cisplatin by Twist siRNA. Altogether, these data suggest that eIF5A2 regulates the resistance of gastric cancer cells to cisplatin by mediating EMT, and support the conclusion that eIF5A2 may be a molecular target for anti-tumor therapy.