PSCA promotes prostate cancer proliferation and cell‐cycle progression by up‐regulating c‐Myc

Li, Ermao; Liu, Luhao; Li, Futian; Luo, Lianmin; Zhao, Shankun; Wang, Jiamin; Kang, Ran; Luo, Jin-Yan; Zhao, Zhigang

doi:10.1002/pros.23432

Cited by 30 publications

(27 citation statements)

References 30 publications

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“…The data from Taeb et al show that expression of PSCA increased from benign prostate tissues (BPH) and HGPIN to prostate cancer and that its expression in prostate cancer was positively associated with poor cell differentiation in Iran [ 30 ]. Similar to these results, our previous studies also revealed that PSCA can promote prostate cancer proliferation and cell-cycle progression and can increase the metastatic potentials by EMT in prostate cell lines [ 15 , 31 ].…”

Section: Discussionsupporting

confidence: 88%

“…Shorter OS was also found in patients with intensive expression of PSCA. As shown in some previous studies, PSCA can promote prostate cancer cell proliferation and escalate the distant metastasis of prostate cancer [ 15 , 31 ]. Therefore, PSCA may play a carcinogenesis role in the progression of prostate cancer, and its expression level in prostate cancer sections might be a useful parameter for judging the prognosis of patients with prostate cancer.…”

Section: Discussionmentioning

confidence: 75%

“…Formalin-fixed and paraffin-embedded consecutive sections from 118 patients who received Transurethral Resection of the Prostate (TURP) ( n = 47) or prostatectomy ( n = 71) from 2009 to 2019 at our hospital were used in the study. Seventy-eight patients were part of a previous study [ 15 ]; however, IHC analyses for those cases were remade and scored with the entire cohort. Patients ranged in age from 42 to 87 years; the mean age was 71.10 ± 9.60 years old.…”

Section: Methodsmentioning

confidence: 99%

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The Correlation between PSCA Expression and Neuroendocrine Differentiation in Prostate Cancer

Xiang

Zhu

Luo

et al. 2020

BioMed Research International

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The prostate stem cell antigen (PSCA), as a predominantly prostate-specific marker, is overexpressed in most prostate cancer specimens, is positively correlated with prostate cancer androgen independence, and has the potential to be treated with castration-resistant prostate cancer (CRPC) as a gene therapy target. Using the typical androgen deprivation therapy, most tumors will progress to CRPC, as well as develop into neuroendocrine prostate cancer (NEPC) characterized by the expression of neuroendocrine markers such as enolase 2 (NSE). Our study was aimed at investigating the expressions of PSCA and NSE and the relationship between the two markers, as well as the correlation between the PSCA and NSE expressions and the clinicopathological parameters in prostate cancer specimens from 118 patients by using immunohistochemistry. Our results demonstrated that the PSCA and NSE protein expressions did not correlate with the prostate cancer patients’ age or the hormone therapy but showed a significant correlation with the pathological tumor stage of prostate cancer, the Gleason score, and the presence of metastasis. There is a positive association between PSCA and NSE but a negative one between the prostate-specific antigen (PSA) and PSCA or between PSA and NSE. High PSCA and NSE expressions correlated with a poor prognosis in prostate cancer patients. PSCA may play an important role in the progression of neuroendocrine prostate cancer (NEPC).

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 75%

Section: Methodsmentioning

confidence: 99%

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The Correlation between PSCA Expression and Neuroendocrine Differentiation in Prostate Cancer

Xiang

Zhu

Luo

et al. 2020

BioMed Research International

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“…c-Myc plays an important role in regulating cell proliferation, differentiation, and apoptosis [ 4 ]. Li et al revealed that the PI3K/AKT signaling pathway was involved in PSCA-promoted cell proliferation and cell cycle progression by upregulating c-Myc in prostate cancer [ 17 ]. Moreover, the previous work demonstrated that c-Myc functions in pancreatic cancer as a central oncogene [ 4 ].…”

Section: Discussionmentioning

confidence: 99%

EI24 Suppresses Tumorigenesis in Pancreatic Cancer via Regulating c-Myc

Zang

Zhu

et al. 2018

Gastroenterology Research and Practice

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The EI24 autophagy-associated transmembrane protein is frequently associated with tumor growth and patient survival. In the present study, we found that EI24 was downregulated in pancreatic ductal adenocarcinoma (PDAC) tissues compared with adjacent normal tissues and was associated with cancer cell differentiation. Overexpression of EI24 suppressed cancer cell growth in vitro and in vivo and induced cell cycle S phase arrest, with no impact on caspase-dependent apoptosis. EI24 overexpression also resulted in reduced c-Myc expression, an oncogene in PDAC, accompanied with increased LC3B-II formation, increased Beclin-1, and diminished p62. Together, we propose that EI24 suppresses cell proliferation and prompts cell cycle arrest in pancreatic cancer cells by activating the autophagic lysosomal degradation of c-Myc. Our results suggest a potential mechanism underlying the antitumor effects of EI24 in PDAC and provide insight into the crosstalk between autophagy and cell proliferation involving a possible EI24/Beclin-1/p62/c-Myc signaling pathway.

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“…Semaphorin 7A (SEMA7A), a GPI-AP, has been found to promote EGFR-tyrosine kinase inhibitor (TKI) resistance in EGFR-mutated lung cancer through activating the mTOR pathway [6]. Prostate stem cell antigen (PSCA), another type of GPI-AP, has been indicated to play an important role in tumorigenesis, proliferation and cell cycle progression via the upregulation of c-Myc expression [7]. In addition, alkaline phosphatase (ALP), glypican-3 (GPC3), and carcinoembryonic antigen (CEA) have been identified as biomarkers of cancers [8–10].…”

Section: Introductionmentioning

confidence: 99%

GPAA1 promotes gastric cancer progression via upregulation of GPI-anchored protein and enhancement of ERBB signalling pathway

Zhang

et al. 2019

J Exp Clin Cancer Res

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Background Gastric cancer is one of the deadliest malignant tumours, with a high incidence in China, and is regulated by aberrantly overexpressed oncogenes. However, existing therapies are insufficient to meet patients’ needs; thus, the identification of additional therapeutic targets and exploration of the underlying mechanism are urgently needed. GPAA1 is the subunit of the GPI transamidase that transfers the GPI anchor to proteins within the ER. The functional impacts of increased expression levels of GPAA1 in human cancers are not well understood. Methods Data mining was performed to determine the pattern of GPAA1 expression and the reason for its overexpression in tumour and adjacent normal tissues. In vitro and in vivo experiments evaluating proliferation and metastasis were performed using cells with stable deletion or overexpression of GPAA1. A tissue microarray established by the Ren Ji Hospital was utilized to analyse the expression profile of GPAA1 and its correlation with prognosis. Western blotting, an in situ proximity ligation assay, and co-immunoprecipitation (co-IP) were performed to reveal the mechanism of GPAA1 in gastric cancer. Results GPAA1 was a markedly upregulated oncogene in gastric cancer due to chromosomal amplification. GPAA1 overexpression was confirmed in specimens from the Ren Ji cohort and was associated with ERBB2 expression, predicting unsatisfactory patient outcomes. Aberrantly upregulated GPAA1 dramatically contributed to cancer growth and metastasis in in vitro and in vivo studies. Mechanistically, GPAA1 enhanced the levels of metastasis-associated GPI-anchored proteins to increase tumour metastasis and intensified lipid raft formation, which consequently promoted the interaction between EGFR and ERBB2 as well as downstream pro-proliferative signalling. Conclusions GPAA1 facilitates the expression of cancer-related GPI-anchored proteins and supplies a more robust platform—the lipid raft—to promote EGFR-ERBB2 dimerization, which further contributes to tumour growth and metastasis and to cancer progression. GPAA1 could be a promising diagnostic biomarker and therapeutic target for gastric cancer. Electronic supplementary material The online version of this article (10.1186/s13046-019-1218-8) contains supplementary material, which is available to authorized users.

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PSCA promotes prostate cancer proliferation and cell‐cycle progression by up‐regulating c‐Myc

Abstract: PSCA is a novel cell cycle regulator with a key role in mediating c-Myc-induced proliferation. PSCA may be a potential diagnostic marker and therapeutic target for patients with PCa.

Cited by 30 publications

References 30 publications

The Correlation between PSCA Expression and Neuroendocrine Differentiation in Prostate Cancer

The Correlation between PSCA Expression and Neuroendocrine Differentiation in Prostate Cancer

EI24 Suppresses Tumorigenesis in Pancreatic Cancer via Regulating c-Myc

GPAA1 promotes gastric cancer progression via upregulation of GPI-anchored protein and enhancement of ERBB signalling pathway

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