Hydroxychloroquine Blocks Autophagy and Promotes Apoptosis of the Prostate after Castration in Rats.

Autophagy is an important pro-survival mechanism and closely related to apoptosis. The aim of this study was to investigate whether hydroxychloroquine (HCQ) blocks autophagy and promotes apoptosis of the prostate after castration. METHODS: Thirty-six male SD rats were randomly divided into 3 groups (n = 12): control group (sham operation), castration group, and HCQ group (castrated and treated with HCQ). On day 7, all mice were executed and prostates were isolated. The morphological changes of prostates were observed by light microscope, and the ultrastructure changes were observed under scanning electron microscope (SEM). The protein expression of Beclin-l, P62, caspase-3, Bcl-2, and Bax was assessed by immunohistochemical analyses. The mRNA expression of microtubule-associated protein light chain 3 (LC3) and autophagy-related gene 5 (Atg5) was detected by RT-PCR. RESULTS: Prostates of castration group shrank remarkably and prostates of HCQ group shrank more remarkably than castration group. Cytolysosomes were visible in the prostates of the castration group under SEM. Immunohistochemistry showed that the protein of Beclin-1 increased in the castration group compared to the control group, while decreased in the HCQ group compared to the castration group. While P62 protein moderately dyed in the control group and weakly dyed in the castration group, it strongly dyed in the HCQ group. Caspase-3 and Bax protein were weakly dyed in the control group but moderately dyed in the castration group and strongly dyed in the HCQ group. The expressions of apoptosis suppressor Bcl-2 were reduced in the castration group and further reduced in the HCQ group compared to the castration group. RT-PCR revealed that the mRNA of LC3 and Atg5 in the castration group increased compared to the control group, while decreased after treated with HCQ. CONCLUSION: Autophagy increased after castrated in prostates, while decreased after treated with HCQ; all these indicated that HCQ blocked autophagy and then promoted prostate apoptosis of castrated mice.

Retraction Note to: MicroRNA-23 regulates the growth, metastasis and chemosensitivity of human gastric cancer cells by targeting MAP3K9.

Retraction of "MicroRNA-23 regulates the growth, metastasis and chemosensitivity of human gastric cancer cells by targeting MAP3K9", by Deping Li, Juan Wang, Yuanjian Hui, Yan Yang, Xingchun Peng, Shengbao Li, Chuantao Sun. JBUON 2020;25(5):2315-2321; PMID: 33277851 Following the publication of the above article, readers drew to our attention that part of the data was unreliable: Figures of this article appeared in other articles (by totally different authors). The authors were requested to provide the raw data and were also asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. Given above, we decided to retract this article. Authors were informed of the retraction. We thank the readers for bringing this matter to our attention. We apologize for any inconvenience it may cause.

MicroRNA-23 regulates the growth, metastasis and chemosensitivity of human gastric cancer cells by targeting MAP3K9.

PURPOSE: The efficient therapeutic targets which could be utilized for gastric cancer are limited. In this context, this study was undertaken to evaluate possible anticancer activity of miR-23 against gastric cancer. METHODS: The normal GES-1 and human AGS, SNU-1 and SNU-5 gastric cancer cells were used in this study. qRT-PCR was used for the determination of miR-23 expression. MTT assay was used for cell viability and acridine orange (AO)/ethidium bromide (EB) assay was used for detection of apoptosis. The experiments were performed in triplicate. RESULTS: The microRNA (miR)-23 was downregulated in gastric cancer cells and showed inhibitory effect on cell growth which was manifested as decline in cell survival. Additionally, the chemosensitivity of gastric cancer cells to cisplatin was enhanced with miR-23 overexpression. Furthermore, miR-23 also inhibited the migration and invasion of cancer cells. MAP3K9 was shown to be the target gene of miR-23 and silencing of MAP3K9 was seen to mimic the growth inhibitory effect of miR-23. Overexpression of MAP3K9 reversed the growth inhibition in miR-23 mimics transfected gastric cancer cells. CONCLUSION: miR-23 exerts growth inhibitory effect against gastric cancer cells and negatively regulates the cell migration and invasion along with enhancement of chemosensitivity of cancer cells.

Curative effect of endostar combined with oxaliplatin in the treatment of primary hepatic carcinoma and its influence on immune cells.

Curative effect and adverse reactions of oxaliplatin combined with endostar in the interventional treatment of primary hepatic carcinoma (PHC) were investigated. A total of 101 PHC patients from October 2012 to December 2014 in The First Affiliated Hospital of Xi'an Jiaotong University were retrospectively collected. Fifty patients in combined therapy group were treated with oxaliplatin combined with endostar, while the remaining 51 patients in oxaliplatin group were treated with oxaliplatin alone. The treatment lasted for a total of 4 cycles (20 days as 1 cycle). The ratios of cluster of differentiation 3 (CD3)+, CD4+ and CD8+ were detected via enzyme-linked immunosorbent assay (ELISA). The objective response rate in combined therapy group was 92.00%, which was significantly higher than that in oxaliplatin group (74.51%). The main adverse reactions showed no statistical difference between the two groups (P>0.05). The median progression-free survival (PFS) was 8.6 months in combined therapy group and 6.3 months in oxaliplatin group, while the median overall survival (OS) was 12.9 months in combined therapy group and 10.6 months in oxaliplatin group. After treatment, CD4+ and CD3+ levels in the peripheral blood in both groups were obviously lower than those before treatment, but the CD8+ level was obviously higher than that before treatment. At the same time, changes in the ratio of T lymphocyte subsets in combined therapy group were superior to those in oxaliplatin group, displaying statistically significant differences (P<0.05). Oxaliplatin combined with endostar has a good curative effect in the treatment of PHC with mild adverse reactions, which can prolong the survival time of patients, improve the levels of T lymphocyte subsets and increase the immunity of patients, so it is worthy of promotion and application in clinic.

The potential role of P.gingivalis in gastrointestinal cancer: a mini review.

Bacterial infection may be involved in the entire process of tissue carcinogenesis by directly or indirectly affecting the occurrence and development of tumors. Porphyromonas gingivalis (P.gingivalis) is an important pathogen causing periodontitis. Periodontitis may promote the occurrence of various tumors. Gastrointestinal tumors are common malignant tumors with high morbidity, high mortality, and low early diagnosis rate. With the rapid development of molecularbiotechnology, the role of P.gingivalis in digestive tract tumors has been increasingly explored. This article reviews the correlation between P.gingivalis and gastrointestinal cancer and the pathogenesis of the latter. The relationship among P.gingivalis, periodontal disease, and digestive tract tumors must be clarifiedthrough a multi-center, prospective, large-scale study.

SIRS-SS: a system for simulating IR/Raman spectra. 2. Procedures and performance.

This paper is devoted to the description of procedures used in our IR/RAMAN spectrum simulation system, based on substructure/subspectrum correlations established between linked databases. The search is performed in the following order: small molecules/specific fragments/atom centered FRELs (FREL: FRagment centered on an Environment which is Limited)/bond focused FRELs. Comparative study with several reported methods has been carried out to show good performance of this software both for IR and RAMAN spectrum simulation.