Clinical Application of Noninflating Video-Endoscopic Inguinal Lymph Node Dissection.

Objective: To assess the safety and efficacy of the application of self-made non-inflating suspension technique in video endoscopic inguinal lymph node dissection (ILND). Methods: We collected 8 patients with penile carcinoma who underwent noninflating video-endoscopic ILND in the Department of Urology, the First Affiliated Hospital of Anhui Medical University, from May 2019 to March 2021. Then, surgical duration, blood loss, drainage tube indwelling time, hospital stay, number of dissected lymph nodes, and complications in the patients were analyzed. Results: All patients (n = 8) finished the surgery successfully, with an average surgical duration of 125 (105-145) minutes, blood loss of 41 (25-50) mL, indwelling time of drainage tube of 7 (5-12) days, and a hospital stay of 14.8 (9-21) days. Additionally, 8.8 (3-14) left side and 7.3 (2-17) right side lymph nodes were dissected on average. Complications occurred in 3 patients during a perioperative period. The patients were followed up for 6-24 months, and none suffered recurrence or metastasis. Conclusion: The efficacy of noninflating video-endoscopic ILND is good. Patients who have undergone the surgery not only have few postoperative complications but also have a good prognosis, suggesting the safety and availability of the clinical application.

Exosomal LINC00355 derived from cancer-associated fibroblasts promotes bladder cancer cell proliferation and invasion by regulating miR-15a-5p/HMGA2 axis.

We have previously demonstrated that exosomes derived from cancer-associated fibroblasts (CAFs) promote bladder cancer (BC) cell proliferation and invasion by transferring LINC00355. In this study, the molecular mechanisms underlying the pro-bladder cancer action of exosomal LINC00355 were explored. CAFs were obtained from BC tumor tissues, and normal fibroblasts (NFs) were obtained from adjacent normal tissues. Human BC cell lines (T24 and 5367) were incubated with NF-Exo (exosomes from NFs), CAF-Exo (exosomes from CAFs), CAFsi-Ctrl-Exo (exosomes from si-Ctrl-transfected CAFs), and CAFsi-LINC00355-Exo (exosomes from si-LINC00355-transfected CAFs). BC cell proliferation and invasion were evaluated by MTT and Transwell assays, respectively. The interaction between miR-15a-5p and LINC00355 or HMGA2 was examined by online bioinformatics analysis and luciferase activity assay. Results showed that HMGA2 is a direct target of miR-15a-5p, and LINC00355 functions as a sponge of miR-15a-5p to upregulate HMGA2 expression. The promoting effects of CAF-Exo on HMGA2 expression, cell proliferation, and cell invasion were hindered when LINC00355 expression was inhibited in BC cells. These promoting effects were also hindered when miR-15a-5p was overexpressed or HMGA2 was silenced in BC cells. In conclusion, exosomal LINC00355 derived from CAFs promotes BC cell proliferation and invasion by regulating miR-15a-5p/HMGA2 axis.

Exosomal LINC00355 derived from cancer-associated fibroblasts promotes bladder cancer cell resistance to cisplatin by regulating miR-34b-5p/ABCB1 axis.

Cisplatin resistance is a major challenge for bladder cancer (BC). Evidence indicates that exosome derived from cancer-associated fibroblasts (CAF-Exo) can promote chemotherapy resistance in various human tumors by delivering bioactive molecules. We have previously demonstrated that CAF-derived exosomal LINC00355 promotes BC cell proliferation and invasion. However, the underlying mechanisms are still unclear. In this study, we aimed to investigate the role and mechanisms of CAF-derived exosomal LINC00355 in BC cell resistance to cisplatin. Exosomes were isolated from normal fibroblasts (NFs) and BC tumor-derived CAFs, namely, NF-Exo and CAF-Exo. CAFs were transfected with si-Ctrl or si-LINC00355 and then different exosomes were isolated, namely, CAFsi-Ctrl-Exo and CAFsi-LINC00355-Exo. The human BC cell lines (T24 and 5367) were incubated with NF-Exo, CAF-Exo, CAFsi-Ctrl-Exo, and CAFsi-LINC00355-Exo in the presence of cisplatin. MTT proliferation assay and flow cytometric analysis showed that CAF-Exo promoted BC cell resistance to cisplatin and upregulated ABCB1 expression in BC cells by transferring LINC00355 to BC cells. Luciferase activity assay confirmed the interaction between miR-34b-5p and LINC00355 or ABCB1. qRT-PCR and western blot analysis further showed that LINC00355 sponged miR-34b-5p to upregulate ABCB1 expression. However, the promoting effects of CAF-Exo on BC cell resistance to cisplatin were abolished by miR-34b-5p overexpression and ABCB1 silencing. In conclusion, exosomal LINC00355 derived from CAFs promotes BC cell resistance to cisplatin by regulating the miR-34b-5p/ABCB1 axis.