Hyperglycaemia promotes the development of Prostate cancer (PCa). However, the roles of miRNAs in this disease process and the underlying mechanisms are largely unknown. In this study, we recruited 391 PCa patients in China and found that PCa patients with high level blood glucose (≥100 mg/dL) trended to have high Gleason score (GS ≥ 7). miRNA-301a levels were significantly higher in prostate cancer than that in normal prostate tissues. Hyperglycaemia or high glucose treatment induced miR-301a expression in prostate tissues or PCa cell lines. miR-301a suppressed the expression of p21 and Smad4, and subsequently promoted G1/S cell cycle transition and cell proliferation in vitro and xenograft growth in nude mice in vivo. Furthermore, knockdown of p21 and Smad4 mimicked the effects of miR-301a overexpression. Restoration of p21 and smad4 could interrupt the effects of miR-301a overexpression. Importantly, inhibition of miR-301a severely blocked high glucose-induced PCa cell growth both in vitro and in vivo. These results revealed a novel molecular link between hyperglycaemia and PCa. The miR-301a plays an important role in the hyperglycaemia-associated cancer growth, and represents a novel therapeutic target for PCa.

This article has been retracted at the request of: Editor-in-Chief and Authors Cross-talk of alpha tocopherol-associated protein and JNK controls the oxidative stress-induced apoptosis in prostate cancer cells' by Baoyi Zhu, Xiaojuan Li, Yuying Zhang, Chunwei Ye, Yu Wang, Songwang Cai, Huaiqiu Huang, Yi Cai, Shuyuan Yeh, Zhenhua Huang, Ruihan Chen, Yiran Tao and Xingqiao Wen The above article, published online on 28 November 2012 in Wiley Online Library (), has been retracted by agreement between the authors, the journal Editor-in-Chief, Prof. Peter Lichter, and Wiley Periodicals, Inc. The Retraction has been agreed due to errors that were detected in Fig. 6b. Some images were duplicated and erroneously presented as unique. Although the authors firmly stand by the major conclusion of this paper, they believe the most responsible course of action is to retract it. Reference Zhu, B., Li, X., Zhang, Y., Ye, C., Wang, Y., Cai, S., Huang, H., Cai, Y., Yeh, S., Huang, Z., Chen, R., Tao, Y. and Wen, X. (2013), Cross-talk of alpha tocopherol-associated protein and JNK controls the oxidative stress-induced apoptosis in prostate cancer cells. Int. J. Cancer, 132: 2270-2282. doi: 10.1002/ijc.27927

A 63-year-old male presented with lower abdominal pain and oliguria due to a large mass in the seminal vesicles. Positron emission tomography/CT (PET/CT) examination showed multiple lesions in the seminal Vesicles, parapharyngeal space, mediastinum and spermatic cord. The result of transrectal ultrasound (TRUS)-guided biopsy indicated a diffuse, large, B-cell lymphoma of the seminal vesicles. PET-CT and TRUS guided biopsy were very helpful to make the correct diagnosis of this unique case.

Excess intracellular reactive oxygen species (ROS) beyond a threshold can induce apoptosis in cancer cells. However, the signal pathways that can augment the proapoptotic function of ROS remain largely unknown. We previously identified a tumor suppressor, alpha‐tocopherol‐associated protein (TAP), yet little is known regarding the role of TAP in the apoptotic signaling in prostate cancer. Interestingly, we recently found that exposure of prostate cancer cells to hydrogen peroxide (H 2 O 2 ) resulted in induced apoptosis as well as increased expression of TAP. Small interfering RNA (siRNA) mediated silencing of endogenous TAP expression conferred effective protection from H 2 O 2 ‐induced apoptosis. Further mechanistic study showed exposure of prostate cancer cells to H 2 O 2 resulted in increased phosphorylation of both JNK and c‐Jun, and TAP siRNA effectively decreased H 2 O 2 ‐induced JNK and c‐Jun phosphorylation. Immunoprecipitation experiments revealed that JNK physically associates with TAP. Furthermore, signaling downstream of JNK to the AP‐1 complex and BH‐3‐only subfamily were found to be regulated on changing the TAP expression status. TAP could also promote the oxidative stress‐induced apoptosis effect of docetaxel. In the mice xenograft model, H 2 O 2 treatment induced TAP expression, JNK phosphorylation and apoptosis of prostate cancer. Recombinant adeno‐associated virus 2 (rAAV2)‐TAP injection significantly sensitizes this H 2 O 2 proapoptotic effect. Together, we have identified a novel functional mechanism that the cross‐talk of TAP‐JNK is involved in oxidative stress‐induced apoptosis in prostate cancer cells. Disrupting the redox balance of cancer cells by this signaling may enable therapeutic selectivity and provide benefit to overcome the drug resistance of prostate cancer.