PSMD11, PTPRM and PTPRB as novel biomarkers of pancreatic cancer progression

Sahni, Sumit; Molloy, Mark P.; Nahm, Christopher B.; Maloney, Sarah; Gillson, Josef; Gill, Anthony J.; Samra, Jaswinder S.; Mittal, Anubhav

doi:10.1016/j.bbagen.2020.129682

Cited by 20 publications

(14 citation statements)

References 47 publications

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“…Although the pro-thrombotic environment of many cancers is rich in fibrin ( 305 ), future studies are required to evaluate whether levels of sGPVI can be also a diagnostic tool to predict thrombosis and correlated to the cancer stage. GPVI would also represent a prognostic marker in pancreatic adenocarcinoma since elevated levels of GPVI were detected in microparticles isolated from patient blood ( 306 ). Further studies are required to define whether some of the above-indicated platelet-derived molecules can be universal diagnostic/prognostic markers for cancers or only specific of a particular cancer type.…”

Section: P Selectinmentioning

confidence: 99%

Platelet-Cancer Interplay: Molecular Mechanisms and New Therapeutic Avenues

et al. 2021

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Although platelets are critically involved in thrombosis and hemostasis, experimental and clinical evidence indicate that platelets promote tumor progression and metastasis through a wide range of physical and functional interactions between platelets and cancer cells. Thrombotic and thromboembolic events are frequent complications in patients with solid tumors. Hence, cancer modulates platelet function by directly inducing platelet-tumor aggregates and triggering platelet granule release and altering platelet turnover. Also, platelets enhance tumor cell dissemination by activating endothelial cell function and recruiting immune cells to primary and metastatic tumor sites. In this review, we summarize current knowledge on the complex interactions between platelets and tumor cells and the host microenvironment. We also critically discuss the potential of anti-platelet agents for cancer prevention and treatment.

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Section: P Selectinmentioning

confidence: 99%

Platelet-Cancer Interplay: Molecular Mechanisms and New Therapeutic Avenues

et al. 2021

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“…Pancreatic resection is still the only curative intent therapy for PDAC patients. However, pancreatic resection is complex and carries with it the risk of major morbidity and mortality (28). Thus, there is a desperate need for investigating the pathogenesis and identifying molecular biomarkers of PDAC to facilitate early diagnosis, prognosis prediction, and the development of effective therapeutic strategies for PDAC patients.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of KLK8 Predicts Poor Prognosis in Pancreatic Cancer

Hua

Liu

et al. 2021

Front. Oncol.

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Pancreatic ductal adenocarcinoma (PDAC) is a growing cause of cancer-related mortality worldwide. Kallikrein-related peptidase 8 (KLK8) has potential clinical values in many cancers. However, the clinicopathological significances of KLK8 in PDAC remain unknown. We explored the relationship of KLK8 to clinicopathological features of PDAC based on public databases. KLK8 expression was examined in human PDAC tissues. Cell proliferation and apoptosis were evaluated in KLK8-overexpressed human pancreatic cancer cell lines Mia-paca-2 and Panc-1. The related signaling pathways of KLK8 involved in pancreatic cancer progression were analyzed by gene set enrichment analysis (GSEA) and further verified in in vitro studies. We found that KLK8 was up-regulated in tumor tissues in the TCGA-PAAD cohort, and was an independent prognostic factor for both overall survival and disease-free survival of PDAC. KLK8 mRNA and protein expressions were increased in PDAC tissues compared with para-cancerous pancreas. KLK8 overexpression exerted pro-proliferation and anti-apoptotic functions in Mia-paca-2 and Panc-1 cells. GSEA analysis showed that KLK8 was positively associated with PI3K-Akt-mTOR and Notch pathways. KLK8-induced pro-proliferation and anti-apoptotic effects in Mia-paca-2 and Panc-1 cells were attenuated by inhibitors for PI3K, Akt, and mTOR, but not by inhibitor for Notch. Furthermore, overexpression of KLK8 in Mia-paca-2 and Panc-1 cells significantly increased epidermal growth factor (EGF) levels in the culture media. EGF receptor (EGFR) inhibitor could block KLK8-induced activation of PI3K/Akt/mTOR pathway and attenuate pro-proliferation and anti-apoptotic of KLK8 in Mia-paca-2 and Panc-1 cells. In conclusion, KLK8 overexpression exerts pro-proliferation and anti-apoptotic functions in pancreatic cancer cells via EGF signaling-dependent activation of PI3K/Akt/mTOR pathway. Upregulated KLK8 in PDAC predicts poor prognosis and may be a potential therapeutic target for PDAC.

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“…Pancreatic resection is still the only curative intent therapy for PDAC patients. However, pancreatic resection is complex and carries with it the risk of major morbidity and mortality [22]. Thus, there is a desperate need for investigating the pathogenesis and identifying molecular biomarkers of PDAC to facilitate early diagnosis, prognosis prediction, and the development of effective therapeutic strategies for PDAC patients.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of KLK8 Predicts Poor Prognosis in Pancreatic Cancer

Hua

Liu

et al. 2020

Preprint

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Background: Pancreatic ductal adenocarcinoma (PDAC) is a growing cause of cancer-related mortality worldwide. Kallikrein-related peptidase 8 (KLK8) has potential clinical values in many cancers. However, the clinicopathological significances of KLK8 in PDAC remain unknown. Methods: The relationship of KLK8 to clinicopathological features of PDAC was investigated based on public databases. KLK8 expression was examined in human PDAC tissues. Cell proliferation and apoptosis were evaluated in KLK8-overexpressed human pancreatic cancer cell lines Mia-paca-2 and Panc-1. The related signaling pathways of KLK8 involved in pancreatic cancer progression were analyzed by gene set enrichment analysis (GSEA) and further verified in in vitro studies. Results: KLK8 was up-regulated in tumor tissues in the TCGA-PAAD cohort, and was an independent prognostic factor for both overall survival and disease-free survival of PDAC. KLK8 mRNA and protein expressions were increased in PDAC tissues compared with para-cancerous pancreas. KLK8 overexpression exerted pro-proliferation and anti-apoptotic functions in Mia-paca-2 and Panc-1 cells. GSEA analysis showed that KLK8 was positively associated with PI3K-Akt-mTOR and Notch pathways. KLK8-induced pro-proliferation and anti-apoptotic effects in Mia-paca-2 and Panc-1 cells were attenuated by inhibitors for PI3K, Akt, and mTOR, but not by inhibitor for Notch.Conclusion: KLK8 overexpression exerts pro-proliferation and anti-apoptotic functions in pancreatic cancer cells via PI3K/Akt/mTOR pathway. Upregulated KLK8 in PDAC predicts poor prognosis and may be a potential therapeutic target for PDAC.

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PSMD11, PTPRM and PTPRB as novel biomarkers of pancreatic cancer progression

Cited by 20 publications

References 47 publications

Platelet-Cancer Interplay: Molecular Mechanisms and New Therapeutic Avenues

Platelet-Cancer Interplay: Molecular Mechanisms and New Therapeutic Avenues

Upregulation of KLK8 Predicts Poor Prognosis in Pancreatic Cancer

Upregulation of KLK8 Predicts Poor Prognosis in Pancreatic Cancer

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