1.Research advances on prostate cancer related genes.
Chinese Journal of Pathology 2022;51(10):1065-1068
2.Relationship between TMPRSS2: ERG and the pathological grade of prostate cancer.
Fa-xian YI ; Hong LI ; Qiang WEI ; Xiang LI ; Hao ZENG
National Journal of Andrology 2015;21(10):887-891
OBJECTIVETo study the relationship between TMPRSS2: ERG gene fusion and the pathological grade of prostate cancer (PCa).
METHODSWe collected fresh prostatic tissue samples from 62 patients with PCa and another 10 with benign prostatic hyperplasia ( BPH) and included 9 cancer cell strains as the control. We examined the TMPRSS2:ERG fusion gene in the PCa samples by nest RT-PCR, compared the Gleason scores between the TMPRSS2:ERG-positive and -negative cases, and analyzed the association of TMPRSS2: ERG fusion with the pathological features of PCa.
RESULTSThe TMPRSS2: ERG fusion gene was detected in 28 (45.16%) of the PCa cases, but in none of the 10 BPH cases or the 9 cancer cell strains. No statistically significant differences were found in the Gleason scores between the TMPRSS2:ERG-positive and -negative cases (Z = -0.609, P = 0.542), but the primary Gleason score was markedly higher in the former than in the latter (Z = -2.600, P = 0.009). Univariate logistic regression analysis showed that TMPRSS2:ERG was associated with the cribriform growth pattern (OR = 6.250, P = 0.002), foamy gland morphology (OR = 6.666, P = 0.023), and signet-ring cells (OR = 3.240, P = 0.035), but multivariate logistic regression analysis manifested that it was associated with the cribriform growth pattern only (OR = 3.750, P = 0.033).
CONCLUSIONTMPRSS2:ERG gene fusion was associated with higher pathological grades of prostate cancer.
Gene Fusion ; Humans ; Male ; Oncogene Proteins, Fusion ; genetics ; Prostatic Hyperplasia ; genetics ; Prostatic Neoplasms ; genetics ; pathology
3.Correlation of androgen receptor CAG repeats with the risks of benign prostatic hyperplasia and prostate cancer: a meta-analysis.
Xiao-Ming WANG ; Liang SUN ; Zheng ZHANG ; Xiao-Hong SHI ; Yao-Guang ZHANG ; Dong WEI ; Ben WAN ; Ze YANG ; Jian-Ye WANG
National Journal of Andrology 2014;20(2):172-176
OBJECTIVETo explore the association of the androgenic receptor (AR) CAG repeats with the risks of benign prostatic hyperplasia (BPH) and prostate cancer (PCa).
METHODSWe searched the major databases at home and abroad for the literature addressing the correlation of the AR gene CAG repeats with BPH and PCa. Based on the results of heterogeneity tests, we used the M-H fixed effect model and random effect model to pool the odds ratio (OR) effect size. We evaluated publication bias by Begg and Egger bias analysis, investigated the association of CAG repeats with the risks of BPH and PCa by systematic review, and stratified their relationship according to the races of the patients.
RESULTSBased on the selection criteria, 4 of the 29 identified studies were included, with 485 cases of BPH, 767 cases of PCa, and 709 controls. There was no heterogeneity between the BPH and control groups, and no correlation between short CAG repeats and BPH after pooling the odds ratio (OR) effect size. Heterogeneity was found among the BPH, PCa and control groups. Random effects model suggested an association of short CAG repeats with the risk of PCa (OR(PCa/control) = 1.45, OR(PCa/BPH) = 1.86, OR(PCa/(BPH + control)) = 1.66), while subgroup analysis with racial stratification indicated inter-ethnic differences between the two. Begg and Egger bias analysis showed no significant publication bias.
CONCLUSIONShorter CAG repeats are positively correlated with the risk of PCa but not with that of BPH.
Humans ; Male ; Polymorphism, Genetic ; Prostatic Hyperplasia ; genetics ; Prostatic Neoplasms ; genetics ; Receptors, Androgen ; genetics ; Trinucleotide Repeats
4.DNA methylation and prostate cancer.
Shui-Gen ZHOU ; Ying-Hao SUN ; Jian-Ping GAO
National Journal of Andrology 2007;13(12):1108-1112
DNA methylation is a common event in malignancies and implicated in tumor initiation and progression. There is a battery of genes involved in critical cell processes such as DNA damage repair, which are hypermethylated in prostate cancer. DNA methylation has also been found in premalignant lesions such as prostatic intraepithelial neoplasia, but to a less extent compared with that in prostate cancer. Intensive study on DNA methylation would provide a new opportunity for the early diagnosis, prognosis and treatment of prostate cancer.
DNA Methylation
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Humans
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Male
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Prognosis
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Prostatic Neoplasms
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diagnosis
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genetics
5.Single nucleotide polymorphisms and prostate cancer.
Chao MA ; Chun-Xiao LIU ; Peng HUANG
National Journal of Andrology 2014;20(8):738-742
Prostate cancer is a common malignancy that affects men's health in the Western countries. Single nucleotide polymorphisms (SNPs), as the third generation of genetic markers, can influence the development, progression, and prognosis of prostate cancer. The same SNP may be related differently with prostate cancer among different races. This paper describes the relationship between SNPs and prostate cancer according to their related genes. SNPs can predict the risk of prostate cancer as well as the possible adverse reactions in its treatment, but at present they do have some limitations.
Humans
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Male
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Polymorphism, Single Nucleotide
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Prostatic Neoplasms
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genetics
6.LncRNA in prostate cancer: an update.
Xiu-Quan GUO ; Tian LAN ; Yang-Min WANG
National Journal of Andrology 2013;19(9):826-830
Recent studies have demonstrated the importance of the non-protein coding part of human genome in carcinogenesis and metastasis of prostate cancer. Long non-coding RNAs (lncRNAs) play a key regulatory role in prostate cancer biology. LncRNAs are dysregulated in prostate cancer and the expression levels of certain lncRNAs are associated with the recurrence, metastasis and prognosis of cancer. It is also proved that lncRNAs, as oncogenes, can promote carcinogenesis and development of prostate cancer. This review focuses on the progress in the studies of lncRNAs in prostate cancer.
Biomarkers, Tumor
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Humans
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Male
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Prostatic Neoplasms
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genetics
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RNA, Long Noncoding
7.Are we ready for prostate cancer?
Chinese Medical Journal 2008;121(4):291-291
China
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epidemiology
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Humans
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Male
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Prostatic Neoplasms
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epidemiology
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genetics
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surgery
8.Roles of highly expressed bone-specific genes in bone metastatic prostate cancer PC3 cells: Advances in studies.
Shi-Yi ZHOU ; Dong WANG ; Ji-Chun SHAO ; Yao-Dong YOU
National Journal of Andrology 2021;27(10):927-933
Prostate cancer (PCa) is a maligmancy with high morbidity and mortality. Bone metastasis is the main cause of short survival time and difficulties in the treatment and prevention of PCa. Previous findings of our team showed 155 bone-specific genes highly expressed in bone metastatic PC3 cells, which is considered to be the key to their adaptation to the bone micro-environment, proliferation and formation of metastatic tumor, and extensively exists in cancer metastasis in multiple systems. This review summarizes the published literature on the highly expressed bone-specific genes, focusing on the roles and values of these genes in the metastasis, progression, clinical diagnosis, treatment and prognosis of PCa, offering a prospect of the direction and targets in the studies of PCa bone metastasis so as to enrich the bone metastatic theories and clinical treatment principles of this disease in the future.
Humans
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Male
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PC-3 Cells
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Prostatic Neoplasms/genetics*
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Tumor Microenvironment
9.Mechanism of piRNA in bisphenol A-promoted invasion and migration of prostate cancer cells.
Shuai BEN ; Lu Lu FAN ; Yi Fei CHENG ; Gong CHENG ; Shu Wei LI ; Mei Lin WANG
Chinese Journal of Preventive Medicine 2023;57(9):1440-1446
Objective: To investigate the regulatory mechanisms of piwi-interacting RNA (piRNA) in bisphenol A (BPA)-induced prostate cancer cell invasion and migration. Methods: The Cancer Genome Atlas (TCGA) data was used to analyze and screen for piRNAs with significantly increased expression in prostate cancer tissues. PC-3 cells were treated with different concentrations of BPA for 12, 24, and 48 h, respectively, and the 20% inhibitory concentration (IC20) was measured using a CCK-8 assay. The expression levels of piRNAs before and after BPA treatment were determined by reverse transcription-quantitative PCR. Target genes regulated by BPA and associated with prostate cancer were screened in the Comparative Toxicogenomics Database (CTD). Dual-luciferase reporter gene assay was performed to verify the relationship between piRNA and target genes, and the expression change of the piRNA target gene was detected by Western blotting. Cell migration and invasion assays were used to determine the effects of piRNA on the malignant phenotype of prostate cancer cells. Results: After treatment of PC-3 cells with 160 μmol/L BPA, the expression of piR-sno48 was most significantly increased (P<0.05). Transfection of piR-sno48 antagomir resulted in decreased expression of endogenous piR-sno48 and a significant increase in the expression of its target gene GSTP1 (P<0.05). However, the expression of GSTP1 did not change significantly in BPA-treated PC-3 cells after transfection with piR-sno48 antagomir (P>0.05). The dual-luciferase reporter gene confirmed that piR-sno48 inhibited the expression of GSTP1 by forming an inversely complementary sequence with the 3'-UTR of GSTP1. The Transwell assay results showed that treatment with BPA significantly increased the invasion and migration ability of prostate cancer cells (P<0.01), whereas piR-sno48 antagonists significantly inhibited the effects above (P<0.01). Conclusion: BPA promotes the invasion and migration of prostate cancer cells by upregulating the expression of piR-sno48 and suppressing the expression of GSTP1. Interfering with the expression of endogenous piR-sno48 may inhibit the malignant phenotype of prostate cancer cells caused by BPA.
Male
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Humans
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Prostate
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Piwi-Interacting RNA
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Antagomirs
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Prostatic Neoplasms/genetics*
10.Mechanism of piRNA in bisphenol A-promoted invasion and migration of prostate cancer cells.
Shuai BEN ; Lu Lu FAN ; Yi Fei CHENG ; Gong CHENG ; Shu Wei LI ; Mei Lin WANG
Chinese Journal of Preventive Medicine 2023;57(9):1440-1446
Objective: To investigate the regulatory mechanisms of piwi-interacting RNA (piRNA) in bisphenol A (BPA)-induced prostate cancer cell invasion and migration. Methods: The Cancer Genome Atlas (TCGA) data was used to analyze and screen for piRNAs with significantly increased expression in prostate cancer tissues. PC-3 cells were treated with different concentrations of BPA for 12, 24, and 48 h, respectively, and the 20% inhibitory concentration (IC20) was measured using a CCK-8 assay. The expression levels of piRNAs before and after BPA treatment were determined by reverse transcription-quantitative PCR. Target genes regulated by BPA and associated with prostate cancer were screened in the Comparative Toxicogenomics Database (CTD). Dual-luciferase reporter gene assay was performed to verify the relationship between piRNA and target genes, and the expression change of the piRNA target gene was detected by Western blotting. Cell migration and invasion assays were used to determine the effects of piRNA on the malignant phenotype of prostate cancer cells. Results: After treatment of PC-3 cells with 160 μmol/L BPA, the expression of piR-sno48 was most significantly increased (P<0.05). Transfection of piR-sno48 antagomir resulted in decreased expression of endogenous piR-sno48 and a significant increase in the expression of its target gene GSTP1 (P<0.05). However, the expression of GSTP1 did not change significantly in BPA-treated PC-3 cells after transfection with piR-sno48 antagomir (P>0.05). The dual-luciferase reporter gene confirmed that piR-sno48 inhibited the expression of GSTP1 by forming an inversely complementary sequence with the 3'-UTR of GSTP1. The Transwell assay results showed that treatment with BPA significantly increased the invasion and migration ability of prostate cancer cells (P<0.01), whereas piR-sno48 antagonists significantly inhibited the effects above (P<0.01). Conclusion: BPA promotes the invasion and migration of prostate cancer cells by upregulating the expression of piR-sno48 and suppressing the expression of GSTP1. Interfering with the expression of endogenous piR-sno48 may inhibit the malignant phenotype of prostate cancer cells caused by BPA.
Male
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Humans
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Prostate
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Piwi-Interacting RNA
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Antagomirs
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Prostatic Neoplasms/genetics*