Regulation of the tumor suppressor PTEN in triple-negative breast cancer

Chai, Chee‐Yin; Wu, Hong; Abuetabh, Yasser; Sergi, Consolato; Leng, Roger

doi:10.1016/j.canlet.2021.12.003

Cited by 41 publications

(37 citation statements)

References 112 publications

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“…A previous study has shown similar PTEN loss of expression findings, observed in 7.4% of breast cancer patients [ 20 ]. Some studies have reported that PTEN gene mutations occurr in 5% to 10%, which is in line with our findings in the present study [ 21 , 22 ]. PTEN immunoexpression loss usually correlates with more significant tumor sizes, multiple lymph node metastases, and an aggressive triple-negative phenotype [ 23 ].…”

Section: Discussionsupporting

confidence: 94%

Patterns of Immunohistochemical Expression of P53, BCL2, PTEN, and HER2/neu Tumor Markers in Specific Breast Cancer Lesions

Bealy

Abugooda

Ahmed

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Objective. This study aimed to associate the expression of P53, BCL2, PTEN, and HER2/neu tumor markers in specific breast cancer lesions. Methods. This study analyzed the immunohistochemical expression of P53, BCL2, PTEN, and HER2/neu tumor markers for 306 patients who presented with lesions. Tissue blocks and patients’ identification data were retrieved from the department of pathology, AL Madinah Almonwarah hospital, Al Madinah, UAE. Results. Of the 306 patients, 104 had benign lesions and 202 had malignancy (including 194 females and 6 males). Most females were presented with invasive ductal carcinoma (IDC), followed by infiltrating ductal carcinoma, and invasive lobular carcinoma (ILC), representing 70%, 23.2%, and 3.7%, respectively. Positive P53, BCL2, PTEN, and HER2 were identified in 20.8%, 11.9%, 91%, and 18.3%, respectively. Conclusion: The expression of P53, BCL2, PTEN, and HER2/neu tumor markers among Saudi patients with breast cancer is relatively similar in many parts of the world.

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Section: Discussionsupporting

confidence: 94%

Patterns of Immunohistochemical Expression of P53, BCL2, PTEN, and HER2/neu Tumor Markers in Specific Breast Cancer Lesions

Bealy

Abugooda

Ahmed

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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“…Recently, accumulating research suggest PTEN plays a pivotal role in the occurrence and development of tumors [34][35][36]. So far, many of PTEN related downstream catalytic functions have been identi ed [37][38][39].…”

Section: Discussionmentioning

confidence: 99%

Estrogen regulates PTEN to induce epithelial ovarian cancer cell proliferation using a two-pronged approach: genomic pathway and non-genomic pathway

Miao

Wang

et al. 2022

Preprint

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Background Epithelial ovarian cancer (EOC) has the highest mortality rate among malignant tumors in women and its occurrence and development are strongly linked to estrogen. Having identified the phosphatase and tensin homologue (PTEN) is a potent tumor suppressor regulating cell proliferation, migration, and survival. Although the role of PTEN in inhibiting cancer has long been emphasized, the role in estrogen-induced EOC is unclear. Results We got the following main results. (1) PTEN expression is decreased in EOC tissues. (2) Estrogen decreased PTEN expression in EOC cells via the estrogen receptor ESR1. (3) Knockdown of PTEN enhanced the proliferation and migration of SK-OV-3 cells by estrogen. (4) Estrogen induced phosphorylation of PTEN via the G-protein-coupled receptor (GPCR)-Protein kinase C (PKC) non-genomic pathway. (5) Inhibiting the phosphorylation of PTEN weakened the proliferation and migration of SK-OV-3 cells by estrogen and decreased the phosphorylation of AKT and mammalian target of rapamycin (mTOR). Conclusion The data indicated that estrogen decreased PTEN expression level via the ESR1 genomic pathway and phosphorylated PTEN via the GPCR-PKC non-genomic pathway to activate the PI3K/AKT/mTOR signaling pathway, thereby determining the fate of epithelial ovarian cancer cells.

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“…PTEN is among the most frequently inactivated tumor suppressor genes in sporadic cancer 46 . The tumor suppressor activity of PTEN is dependent on its lipid phosphatase activity, which negatively regulates the PI3K/Akt pathway 48 . Even a subtle decrease in PTEN levels and activity results in cancer susceptibility and favors tumor progression and migration 46 .…”

Section: Discussionmentioning

confidence: 99%

Tetrachlorobisphenol A and bisphenol AF induced cell migration by activating PI3K/Akt signaling pathway via G protein‐coupled estrogen receptor 1 in SK‐BR‐3 cells

Lei

et al. 2022

Environmental Toxicology

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Different subtypes of breast cancer express positively G protein‐coupled estrogen receptor 1 (GPER1). Our previous studies found that tetrachlorobisphenol A (TCBPA) and bisphenol AF (BPAF) significantly promoted SK‐BR‐3 cell proliferation by activating GPER1‐regulated signals. The present study further investigated the effects of TCBPA and BPAF on the migration of SK‐BR‐3 cells and examined the role of phosphatidylinositol 3‐kinase‐protein kinase B (PI3K/Akt) and its downstream signal targets in this process. We found that low‐concentration BPAF and TCBPA markedly accelerated the migration of SK‐BR‐3 cells and elevated the mRNA levels of target genes associated with PI3K/Akt and mitogen‐activated protein kinase (MAPK) signals. TCBPA‐ and BPAF‐induced upregulation of target genes was significantly reduced by GPER1 inhibitor G15, the PI3K/Akt inhibitor wortmannin (WM), and the epidermal growth factor receptor (EGFR) inhibitor ZD1839 (ZD). G15 and WM also decreased cell migration induced by TCBPA and BPAF. The findings revealed that TCBPA and BPAF promoted SK‐BR‐3 cell migration ability by activating PI3K/Akt signaling pathway via GPER1‐EGFR.

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Regulation of the tumor suppressor PTEN in triple-negative breast cancer

Cited by 41 publications

References 112 publications

Patterns of Immunohistochemical Expression of P53, BCL2, PTEN, and HER2/neu Tumor Markers in Specific Breast Cancer Lesions

Patterns of Immunohistochemical Expression of P53, BCL2, PTEN, and HER2/neu Tumor Markers in Specific Breast Cancer Lesions

Estrogen regulates PTEN to induce epithelial ovarian cancer cell proliferation using a two-pronged approach: genomic pathway and non-genomic pathway

Tetrachlorobisphenol A and bisphenol AF induced cell migration by activating PI3K/Akt signaling pathway via G protein‐coupled estrogen receptor 1 in SK‐BR‐3 cells

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