Modified versus three-level technique of retroperitoneal laparoscopic adrenalectomy for all patients with adrenal lesions ≤ 6cm: a retrospective, case-controlled study.

Objectives: The modified three-level technique for retroperitoneal laparoscopic adrenalectomy (RLA) has proven beneficial in the treatment of adrenal lesions in patients with BMI≥25 Kg/m2. This paper aims to summarize our institution's seven-year experience using this technique for all patients with Adrenal Lesions ≤ 6cm. Patients and methods: Between January 2016 and December 2022. The patients underwent laparoscopic adrenal surgery were categorized into Zhang's technique (ZT) (Three-level Technique) group and modified technique (MT) group. The fundamental characteristics and perioperative data were analyzed, with statistical significance set at p<0.05. Results: In total, 731 patients were stratified into two groups: ZT (n=448) and MT (n=283). Statistically significant distinctions were not detected between the two groups regarding sex, BMI, tumor location, tumor size, tumor type, or American Society of Anesthesiologists (ASA) score (p>0.05). The MT group demonstrated superior outcomes compared to the ZT group in terms of operative time, estimated blood loss, drainage volume, diet recovery time, complication rates, and postoperative hospitalization duration (p<0.05). 17 (4.34%) in the ZT group required unplanned adrenalectomy, while there was none in MT group (P<0.05). Conclusion: MT retroperitoneal laparoscopic adrenalectomy has demonstrated its benefits in the treatment of adrenal lesions across all patients with adrenal lesions ≤ 6cm, serving as a valuable point of reference for the surgical management of adrenal diseases. Patient summary: We have made modifications to the classic retroperitoneal laparoscopic adrenalectomy and achieved superior surgical outcomes, resulting in a procedure known as modified retroperitoneal laparoscopic adrenalectomy. This technique is suitable for both obese individuals and the general population with adrenal lesions ≤ 6cm.

Upregulation of GRIM-19 augments the sensitivity of prostate cancer cells to docetaxel by targeting Rad23b.

The gene associated with retinoid-interferon mortality (GRIM-19) has been reported to be correlated with drug resistance, whereas its functional role in prostate cancer (PC) is not fully understood. This study aims to clarify the potential role and molecular mechanisms of GRIM-19 on the response of PC cells to chemical drug docetaxel. mRNA and protein level of GRIM-19 expression in cells and tissues of PC were measured by quantitative real-time PCR and western blot, respectively. Knock-down of GRIM-19 in PC cells was performed using siRNA. Cell apoptosis was determined by flow cytometric analysis. DNA damage in PC cells was detected by γ-H2AX staining. GRIM-19 was downregulated in PC tissues and cell lines. Knock-down of GRIM-19 increased the resistance of PC cells to docetaxel, and overexpression of GRIM-19 promoted docetaxel-induced apoptotic death in PC cells. Mechanistically, GRIM-19 downregulated the expression of the survival gene Rad23b, which promoted DNA damage repair. Overexpression of Rad23b reversed GRIM-19-mediated response to docetaxel in PC cells. GRIM-19 promoted the sensitivity of PC cells to docetaxel by downregulating Rad23b, which may serve as a promising target to develop a better strategy of chemotherapy for PC.

Inhibition of miR-423-5p suppressed prostate cancer through targeting GRIM-19.

OBJECTIVE: To determine the effect of miR-423-5p on the progression of prostate cancer (PC). METHODS: miR-423-5p and GRIM-19 expressions were detected by qRT-PCR and western blot. PC cell proliferation was measured by MTT assay. PC cell apoptosis was detected by flow cytometry. Dual luciferase reporter assay was used to confirm the interaction between miR-423-5p and GRIM-19. RESULTS: Compared with normal prostate tissues and prostate epithelial cell HPrEC, miR-423-5p was up-regulated in human PC tissues and PC3 cells, whereas GRIM-19 expression was decreased. Inhibition of miR-423-5p suppressed PC3 cell proliferation, promoted PC3 cell apoptosis, and decreased anti-apoptosis protein BCL-2 expression. GRIM-19 was a target of miR-423-5p, and GRIM-19 was negatively regulated by miR-423-5p in PC3 cells. In addition, miR-423-5p knockdown inhibited the proliferation and promoted the apoptosis of PC3 cells through GRIM-19. In vivo experiments showed that miR-423-5p inhibitor administration reduced tumor volume, down-regulated miR-423-5p and GRIM-19 expressions in PC tissues of nude mice. CONCLUSION: Inhibition of miR-423-5p suppressed PC through targeting GRIM-19.

Notch 1 is a valuable therapeutic target against cell survival and proliferation in clear cell renal cell carcinoma.

Notch 1 is a key component of the Notch pathway, which performs a crucial role in clear cell renal cell carcinoma (CCRCC) development. The present study aimed to investigate whether Notch 1 could serve as a potential target for CCRCC treatment. Firstly, an association analysis was performed using 52 CCRCC cases and 30 normal controls. The results indicated that Notch 1 protein expression in renal tissues was closely associated with the incidence of CCRCC. In addition, higher Notch 1 expression in CCRCC tissues was positively associated with higher tumor-node-metastasis stage and Fuhrman grade, in addition to larger tumor size. Subsequently, an in vitro study was conducted to examine the biological functions of Notch 1 in CCRCC 786-O cells through inhibiting the Notch 1 expression with Notch 1-specific small interfering RNA (siRNA). As a result, the inhibition of Notch 1 expression by increasing concentrations of Notch 1-specific siRNA dose-dependently decreased cell proliferation and increased cell apoptosis in 786-O cells. Furthermore, B-cell lymphoma-2 and procaspase-3 expression exhibited a dose-dependent decrease accompanied with a dose-dependent inactivation of the Akt/mammalian target of rapamycin (mTOR) signaling pathway in Notch 1 siRNA-treated 786-O cells. These findings demonstrated that Notch 1 was associated with CCRCC carcinogenesis and progression, the underlying mechanism of which was that Notch 1 acted as an activator for cell proliferation and a suppressor for cell apoptosis through the Akt/mTOR signaling-dependent pathway in CCRCC. In conclusion, the present study confirmed that Notch 1 is a valuable target against cell survival and proliferation in CCRCC treatment.