Correlation between hypoxia and HGF/c-MET expression in the management of pancreatic cancer

Sharma, Rakesh Chandmal; Malviya, Rishabha

doi:10.1016/j.bbcan.2023.188869

Cited by 5 publications

(2 citation statements)

References 188 publications

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“…The progression of pancreatic cancer involves complex molecular and cellular processes, with distorted autocrine and paracrine signaling pathways playing crucial roles in fostering the growth, migration, invasion, and metastasis of cancer cells. Critical factors, including transforming growth factor-α (TGFα) ( 16 ), insulin-like growth factor 1 (IGF1) ( 17 ), fibroblast growth factors (FGFs) ( 18 ), and hepatocyte growth factor (HGF) ( 19 ), along with their corresponding tyrosine kinase receptors, such as epidermal growth factor receptor (EGFR) ( 20 ), receptor tyrosine-protein kinase erbB-2 (ERBB2/HER2) ( 21 ), HER3 ( 22 ), the IGF1 receptor (IGF1R) ( 23 ), FGF receptors (FGFRs) ( 24 ), and the HGF receptor (HGFR/MET) ( 25 ), trigger several pathways contributing to cell growth ( Figure 1 ).…”

Section: Mechanistic Insightsmentioning

confidence: 99%

Investigating underlying molecular mechanisms, signaling pathways, emerging therapeutic approaches in pancreatic cancer

Mustafa,

Abbas,

Alam

et al. 2024

Front. Oncol.

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Pancreatic adenocarcinoma, a clinically challenging malignancy constitutes a significant contributor to cancer-related mortality, characterized by an inherently poor prognosis. This review aims to provide a comprehensive understanding of pancreatic adenocarcinoma by examining its multifaceted etiologies, including genetic mutations and environmental factors. The review explains the complex molecular mechanisms underlying its pathogenesis and summarizes current therapeutic strategies, including surgery, chemotherapy, and emerging modalities such as immunotherapy. Critical molecular pathways driving pancreatic cancer development, including KRAS, Notch, and Hedgehog, are discussed. Current therapeutic strategies, including surgery, chemotherapy, and radiation, are discussed, with an emphasis on their limitations, particularly in terms of postoperative relapse. Promising research areas, including liquid biopsies, personalized medicine, and gene editing, are explored, demonstrating the significant potential for enhancing diagnosis and treatment. While immunotherapy presents promising prospects, it faces challenges related to immune evasion mechanisms. Emerging research directions, encompassing liquid biopsies, personalized medicine, CRISPR/Cas9 genome editing, and computational intelligence applications, hold promise for refining diagnostic approaches and therapeutic interventions. By integrating insights from genetic, molecular, and clinical research, innovative strategies that improve patient outcomes can be developed. Ongoing research in these emerging fields holds significant promise for advancing the diagnosis and treatment of this formidable malignancy.

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Section: Mechanistic Insightsmentioning

confidence: 99%

Investigating underlying molecular mechanisms, signaling pathways, emerging therapeutic approaches in pancreatic cancer

Mustafa,

Abbas,

Alam

et al. 2024

Front. Oncol.

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“…[11,12] It is found that the hypoxic environment can reduce the chemosensitivity of pancreatic cancer, enhance glycolysis, and improve the immune escape ability through the regulation of signal pathways and gene expression, thus promoting the progress of pancreatic cancer. [13] Therefore, we simulated the hypoxia microenvironment similar to pancreatic cancer to analyze the impact of hypoxia on the progression and gene expression of pancreatic cancer.…”

Section: Introductionmentioning

confidence: 99%

Hypoxia-induced OSBPL10 accelerates pancreatic cancer progression through CNBP sequestration

Huang,

Zhang,

Fan

et al. 2024

Preprint

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Purpose Given oxysterol binding protein like 10’s (OSBPL10) known involvement in lipid transport and oncogenic activity in other tumors, we aimed to elucidate the mechanism underlying its contribution to pancreatic cancer progression. Methods We employed data from the Gene Expression Omnibus database. A series of assays, including CCK8,colony formation,wound healing and transwell, were conducted to assess the impact of OSBPL10 on the proliferation and metastatic capacities of pancreatic cancer cells. Flow cytometry was employed to evaluate the influence of OSBPL10 on macrophages. Co-immunoprecipitation , mass spectrometry, and western blot assays were utilized to investigate the potential mechanisms of OSBPL10 activity. Results The study revealed a significant uoregulation of OSBPL10 in pancreatic cancer cells, correlating with poor prognosis. OSBPL10 knockdown attenuated pancreatic cancer cells proliferation and metastasis, while its overexpression enhanced these malignant behaviors. Notably, OSBPL10 knockdown promoted the transformation of M2 macrophages into M1 macrophages in the pancreatic cancer microenvironment. Mechanistically, hypoxia-induced upregulation of OSBPL10 through interaction with hypoxia-inducible factor 1-α in the promoter region was identified. Additionally, OSBPL10 directly bound to CNBP, mediating CNBP expression and ultimately regulating the proliferation and metastasis capacity of pancreatic cancer cells, as well as influencing macrophage polarization. Conclusions This study provides comprehensive insights into oncogenic role of OSBPL10 in pancreatic cancer, uncovering key mechanisms involving hypoxia, HIF-α,and CNBP. The finding suggest that OSBPL10 plays s crucial role in promoting pancreatic cancer progression, making it a potential therapeutic target for intervention in this malignancy.

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OSBPL10‐CNBP axis mediates hypoxia‐induced pancreatic cancer development

Huang,

Zhang,

Fan

et al. 2024

BioFactors

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Pancreatic ductal adenocarcinoma (PDAC) is one of malignancies with worst outcomes among digestive system tumors. Identification of novel biomarkers is of great significance for treatment researches and prognosis prediction of pancreatic cancer patients. Due to OSBPL10 known involvement in oncogenic activity in other tumors, we elucidated the mechanism underlying its contribution to pancreatic cancer progression. We employed data from the Gene Expression Omnibus database to detect the expression of OSBPL10 in normal and pancreatic cancer tissues. A series of assays were conducted to assess the impact of OSBPL10 on the proliferation and metastatic capacities of pancreatic cancer cells and the influence of OSBPL10 on macrophages were evaluated by Flow cytometry. In addition, Co‐immunoprecipitation, mass spectrometry, and western blot assays were utilized to investigate the potential mechanisms of OSBPL10 activity. From our study, OSBPL10 is revealed to be upregulated in pancreatic cancer, with poor prognosis. The overexpression promotes malignant behaviors of pancreatic cancer cells and has an impact on tumor immune microenvironment by stimulating the transformation M1 macrophages into M2 macrophages. Mechanistically, hypoxia induces the expression of OSBPL10 through interaction between hypoxia‐inducible factor 1‐α and the promoter region of OSBPL10. Additionally, OSBPL10 directly bound to CNBP, mediating CNBP expression and ultimately regulating the proliferation and metastasis capacity of pancreatic cancer cells, as well as influencing macrophage polarization. The research emphasized the oncogenic role of OSBPL10 in pancreatic cancer, uncovering key mechanisms involving hypoxia, HIF‐1α, and CNBP. The finding suggests that OSBPL10 is a novel biomarker in pancreatic cancer, making it a potential therapeutic target for intervention in this malignancy.

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Correlation between hypoxia and HGF/c-MET expression in the management of pancreatic cancer

Cited by 5 publications

References 188 publications

Investigating underlying molecular mechanisms, signaling pathways, emerging therapeutic approaches in pancreatic cancer

Investigating underlying molecular mechanisms, signaling pathways, emerging therapeutic approaches in pancreatic cancer

Hypoxia-induced OSBPL10 accelerates pancreatic cancer progression through CNBP sequestration

OSBPL10‐CNBP axis mediates hypoxia‐induced pancreatic cancer development

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