Expression and clinical significance of Caveolin-1 in prostate Cancer after transurethral surgery

Wang, Xiaoming; Liu, Zhigui; Yang, Zunhua

doi:10.1186/s12894-018-0418-4

Cited by 13 publications

(13 citation statements)

References 31 publications

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“…Cav-1 increases the aggressiveness of cancer cells in pancreatic, hepatic, gastric, and prostate cancers. [28][29][30][31][32][33] However, cav-1 deficiency is seen as a driving force in squamous-cell carcinoma and breast cancer. 34,35 It appears that cav-1 exerts diversified effects in different cancers.…”

Section: Discussionmentioning

confidence: 99%

Caveolin‐1 increases glycolysis in pancreatic cancer cells and triggers cachectic states

et al. 2021

FASEB j.

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In pancreatic cancer, autocrine insulin-like growth factor-1 (IGF-1) and paracrine insulin stimulate both IGF-1 receptor (IGF1R) and insulin receptor (IR) to increase tumor growth and glycolysis. In pancreatic cancer patients, cancer-induced glycolysis increases hepatic gluconeogenesis, skeletal muscle proteolysis, and fat lipolysis and, thereby, causes cancer cachexia. As a protein coexisting with IGF1R and IR, caveolin-1 (cav-1) may be involved in pancreatic cancer-induced cachexia. We undertook the present study to test this hypothesis. Out of wild-type MiaPaCa2 and AsPC1 human pancreatic cancer cell lines, we created their stable sub-lines whose cav-1 expression was diminished with RNA interference or increased with transgene expression. When these cells were studied in vitro, we found that cav-1 regulated IGF1R/IR expression and activation and also regulated cellular glycolysis. We transplanted the different types of MiaPaCa2 cells in growing athymic mice for 8 weeks, using intact athymic mice as tumor-free controls. We found that cav-1 levels in tumor grafts were correlated with expression levels of the enzymes that regulated hepatic gluconeogenesis, skeletal muscle proteolysis, and fat lipolysis in the respective tissues. When the tumors had original or increased cav-1, their carriers' body weight gain was less than the tumor-free reference. When cav-1 was diminished in tumors, the tumor carriers' body weight gain was not changed significantly, compared to the tumor-free reference. In conclusion, cav-1 in pancreatic cancer cells stimulated IGF1R/IR and glycolysis in the cancer cells and triggered cachectic states in the tumor carrier. K E Y W O R D Scancer cachexia, caveolin-1, glycolysis, pancreatic cancer How to cite this article: Hu L, Xu X, Li Q, et al. Caveolin-1 increases glycolysis in pancreatic cancer cells and triggers cachectic states.

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Section: Discussionmentioning

confidence: 99%

Caveolin‐1 increases glycolysis in pancreatic cancer cells and triggers cachectic states

et al. 2021

FASEB j.

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“…Earlier studies indicated that caveolin-1 was related to endocytosis, signaling and lipid disorders, while recent studies focused on clarifying its relevance in cancer. Caveolin-1 is expressed in esophageal carcinoma ( 19 , 20 ), prostate cancer ( 8 – 17 ), colon cancer ( 21 ), breast cancer ( 22 ), bladder cancer ( 23 ), lung cancer ( 24 ), and other cancers ( 25 , 26 ), and acts as a tumor promoter or suppressor. As a tumor promoter, high expression of caveolin-1 drives tumorigenesis by inhibiting apoptosis, facilitating anchorage-independent growth, drug resistance as well as metastasis ( 27 , 28 ).…”

Section: Discussionmentioning

confidence: 99%

“…Based on the inclusion and exclusion criteria, 10 studies (8)(9)(10)(11)(12)(13)(14)(15)(16)(17) were enrolled, which included 3976 cases of prostate cancer, of which 962 were positive for caveolin-1. Moreover, 72 cases were high-grade intraepithelial neoplasia of prostate (HGPIN), of which 15 were positive for caveolin-1.…”

Section: Characteristics Of Enrolled Studiesmentioning

confidence: 99%

“…cancer (8)(9)(10)(11)(12)(13)(14)(15)(16)(17), colon cancer (21), breast cancer (22), bladder cancer (23), lung cancer (24), and other cancers (25,26), and acts as a tumor promoter or suppressor. As a tumor promoter, high expression of caveolin-1 drives tumorigenesis by inhibiting apoptosis, facilitating anchorage-independent growth, drug resistance as well as metastasis (27,28).…”

Section: Figure 4 | Forest Plot On the Comparison Of Caveolin-1 Exprementioning

confidence: 99%

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Association of Caveolin-1 Expression With Prostate Cancer: A Systematic Review and Meta-Analysis

Chen

Zhang

Bai³

et al. 2021

Front. Oncol.

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PurposeThe prognostic value of caveolin-1 in prostate cancer remains uncertain. Hence, this meta-analysis was performed to evaluate the prognostic value of caveolin-1 in prostate cancer, as well as ascertain the relationship between caveolin-1 expression and clinicopathological characteristics of prostate cancer patients.MethodsThe PubMed, Embase, Chinese National Knowledge Infrastructure and Chinese Biology Medicine databases were electronically searched to retrieve published studies on caveolin-1 expression in prostate cancer. After study selection and data extraction, the meta-analysis was conducted using Review manager 5.3 software. Odds ratio (OR) with 95% confidence interval (CI) was used to estimate the pooled effect. Funnel plot was used to assess publication bias.ResultsA total of ten studies were enrolled, which included 3976 cases of prostate cancer, 72 cases of high-grade intraepithelial neoplasia (HGPIN), and 157 normal controls. Results of the meta-analysis showed that the positive rate of caveolin-1 expression in prostate cancer was 18.28 times higher than that in normal control (OR= 18.28, 95% CI: 9.02–37.04, p<0.01), and 4.73 times higher than that in HGPIN (OR= 4.73, 95% CI: 2.38–9.42, p<0.01). The relationship between caveolin-1 and clinicopathological characteristics of prostate cancer showed that the differences in caveolin-1 expression in patients with prostate-specific antigen (PSA) >10 vs. ≤ 10 (OR=2.09, 95% CI: 1.35–3.22, p<0.01), differentiation degree low vs. medium/high (OR=2.74, 95% CI: 1.84–4.08, p<0.01), TNM stage T3+T4 vs. T1+T2 (OR=2.77, 95% CI: 1.78–4.29, p<0.01), and lymph node metastasis present vs. absent (OR=2.61, 95% CI: 1.84–3.69, p<0.01) were statistically significant. The correlation analysis between caveolin-1 and the survival time of patients with prostate cancer demonstrated that caveolin-1 was closely related to the prognosis of prostate cancer patients (HR=1.50, 95% CI: 1.28–1.76, p<0.01).ConclusionCaveolin-1 is overexpressed in prostate cancer, which can serve as a risk factor and adverse clinicopathological feature of prostate cancer. Caveolin-1 can also predict poor survival in prostate cancer patients after radical prostatectomy.

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“…CAV1 is one of the critical components of the integral membrane protein that makes up caveolins. It has been reported to be associated with esophageal carcinoma, [ 15 , 16 ] prostate cancer, [ 17 , 18 ] colon cancer, [ 19 ] breast cancer, [ 20 ] bladder cancer, [ 21 ] lung cancer, [ 22 ] and others, [ 23 , 24 ] which can promote or suppress tumor occurrence and development.…”

Section: Discussionmentioning

confidence: 99%

CAV1 rs7804372 (T29107A) polymorphism might be a potential risk for digestive cancers

Chen¹,

Zhang²,

Bai

et al. 2021

Medicine

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Background: Caveolin-1 (CAV1) is an essential structural component of caveolae, regulates cellular processes through complex cellular signaling pathways, and influences tumorigenicity. However, the role of the CAV1 (rs7804372) polymorphism in digestive cancers remains inconclusive. The meta-analysis was performed to evaluate the effect of CAV1 polymorphism on digestive cancer susceptibility and to provide a basis for precise treatment. Methods: The databases of PubMed, EMBASE, Google Scholar and CNKI were used to retrieve the published studies on CAV1 (rs7804372) polymorphism and susceptibility to digestive cancers up to June 2020. Two researchers conducted study screening, data extraction, and methodological quality evaluation separately according to inclusion and exclusion criteria. Review Manager 5.3 software was used to conduct the meta-analysis. Results: Six case-control studies were enrolled, including 2477 patients with digestive cancers and 2477 healthy controls. The pooled results showed that the CAV1 rs7804372 (T29107A) polymorphism increased the risk of digestive cancer occurrence in the allele ( T vs. A : odds ratio (OR) 1.33, 95% confidence interval (CI): 1.15–1.53, P < .01), homozygous ( TT vs. AA : OR 1.72, 95% CI: 1.31–2.26, P < .01), heterozygous ( TA vs. AA : OR 1.47, 95% CI: 1.21–1.78, P < .01), dominant ( TT vs. TA + AA : OR 1.32, 95% CI: 1.18–1.48, P < .01), and recessive comparing models ( TT + TA vs. AA : OR 1.61, 95% CI: 1.26–2.07, P < .01). Conclusion: Our results indicate that the CAV1 (rs7804372) polymorphism may modify the occurrence of digestive cancers, and the presence of T allele or TT genotype of the CAV1 (rs7804372) may increase the risk of digestive cancers.

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Expression and clinical significance of Caveolin-1 in prostate Cancer after transurethral surgery

Cited by 13 publications

References 31 publications

Caveolin‐1 increases glycolysis in pancreatic cancer cells and triggers cachectic states

Caveolin‐1 increases glycolysis in pancreatic cancer cells and triggers cachectic states

Association of Caveolin-1 Expression With Prostate Cancer: A Systematic Review and Meta-Analysis

CAV1 rs7804372 (T29107A) polymorphism might be a potential risk for digestive cancers

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