Recent studies have reported that TUBB3 overexpression is involved in docetaxel (DTX) resistance in prostate cancer (PCa). The aim of this study was to clarify the role of TUBB3 in DTX and cabazitaxel (CBZ) resistance, and cross-resistance between DTX and CBZ in PCa. We analyzed the effect of TUBB3 knockdown on DTX and CBZ resistance and examined the interaction between TUBB3 and PTEN. We also investigated the role of phosphoinositide 3-kinases (PI3K) inhibitor (LY294002) in DTX and CBZ resistance. TUBB3 expression was upregulated in DTX-resistant and CBZ-resistant cells. TUBB3 knockdown re-sensitized DTX-resistant cells to DTX and CBZ-resistant cells to CBZ. Additionally, TUBB3 knockdown re-sensitized DTX-resistant cell lines to CBZ, indicating that TUBB3 mediates cross-resistance between DTX and CBZ. Knockdown of TUBB3 enhanced PTEN expression, and PTEN knockout enhanced TUBB3 expression. LY294002 suppressed TUBB3 expression in DTX-resistant and CBZ-resistant cell lines. LY294002 re-sensitized DTX-resistant cell lines to DTX and CBZ-resistant cell lines to CBZ. These results suggest that TUBB3 is involved in DTX resistance and CBZ resistance. A combination of LY294002/DTX and that of LY294002/CBZ could be potential strategies for PCa treatment.

Objective: The objective of this study was to identify lymphatic vessels draining from the prostate by using a fluorescence navigation (FN) system. Methods: Fourteen subjects were candidates for radical retropubic prostatectomy (RRP) and pelvic lymph node dissection (PLND). After an indocyanine green solution was injected into the prostate during RRP, lymphatic vessels draining from the prostate were analyzed using a FN system. After PLND based on lymphatic mapping by the FN system (in vivo probing) was performed in the external iliac, obturator and internal iliac regions; the fluorescence of the removed lymph nodes (LNs) was analyzed on the bench (ex vivo probing). Results: Under in vivo and ex vivo probing, the fluorescence intensity of internal iliac nodes was greater than that of external iliac or obturator nodes. Conclusion:The current study suggests that using a FN system after injecting indocyanine green is a safe and rational approach for detecting the lymphatic channel draining from the prostate. The major lymphatic pathway involved in the spreading of prostate cancer appears to relate to internal iliac LNs, which would mean that the standard PLND covering external iliac and obturator regions would not keep the cancer from spreading. RésuméObjectif : L'objectif de l'étude était de repérer les vaisseaux lymphatiques quittant la prostate à l'aide d'un système d'imagerie par fluorescence (IF). Méthodologie : Quatorze sujets devaient subir une prostatectomie radicale rétropubienne (PRR) et une lymphadénectomie pelvienne. Après injection d'une solution de vert d'indocyanine dans la prostate pendant la PRR, les vaisseaux lymphatiques drainant la prostate ont été analysés par IF. Une lymphadénectomie pelvienne fondée sur la cartographie lymphatique par IF (exploration in vivo) a ensuite été réalisée dans les régions de la fosse iliaque externe, de l'obturateur et de la fosse iliaque interne; la fluorescence des ganglions lymphatiques retirés a été analysée sans délai (exploration ex vivo). Résultats : Lors de l'exploration in vivo et ex vivo, l'intensité de la fluorescence des ganglions iliaques internes était plus forte que celle des ganglions iliaques externes ou des ganglions obturateurs. Conclusion : Cette étude porte à croire que l'IF après injection de vert d'indocyanine est une méthode sûre et rationnelle pour repérer les vaisseaux lymphatiques drainant la prostate. La principale voie lymphatique de propagation du cancer de la prostate semble être reliée aux ganglions lymphatiques iliaques internes, ce qui signifie que la lymphadénectomie pelvienne standard retirant les ganglions iliaques externes et obturateurs n'empêcherait pas le cancer de se propager.

Backgrounds: Considering the natural course of cavernous nerve recovery after robot-assisted laparoscopic prostatectomy (RALP), early intervention of low intensity extracorporeal shock wave therapy (LIESWT) would be more effective for enhancing overall recovery of sexual function (SF). Our objective of this study is to analyze longitudinally the alterations of SF in patients after RALP, with a focus on the effect of early and delayed intervention with LIESWT.Methods: A total of 5 and 11 patients underwent early and delayed intervention with LIESWT, respectively. SF was assessed with the Expanded Prostate Cancer Index Composite (EPIC). The same surgeon performed RALP on 178 patients, and these patients were assigned to the non-LIESWT group to establish a control group. The SF score of EPIC was investigated longitudinally before RALP and 3, 6, 9, and 12 months after RALP.Results: Our results show that penile rehabilitation with LIESWT immediately before urethral catheter removal improved SF scores. In the baseline, the SF score was significantly higher in the early LIESWT group (P=0.0001). The SF score was significantly lower at postoperative 6 months (early 19.2, delayed 17.9, and non-LIESWT 8.1; P=0.0171), 9 months (20.9, 25.8, and 10.2; P=0.0188), and 12 months (28.0, 21.3, and 9.5; P=0.0051) in the non-LIESWT group. We regret that there was no significant difference in the recovery of SF between the early and delayed protocol with LIESWT at all points. In keeping with our results, LIESWT demonstrated the potential to be efficacious in treatment options for severe postradical prostatectomy (RP) erectile dysfunction (ED) as it may indirectly support its promotion of nerve regeneration in severe ED due to RP.Conclusions: This is the first study in which LIESWT has been shown to deliver a clinical benefit on its early or delayed intervention to patients after RALP to penile rehabilitation in terms of restoring SF. Our preliminary results suggest that LIESWT could be used as a treatment option in penile rehabilitation.

FGF19 might be associated with biochemical recurrence after radical prostatectomy by promoting cell proliferation and epithelial-mesenchymal transition of PCa.