Integrin β1 in Pancreatic Cancer: Expressions, Functions, and Clinical Implications

Li, Jiajia; Peng, Liyao; Chen, Qun; Ye, Ziping; Zhao, Tiantian; Hou, Sicong; Gu, Jianguo; Hang, Qinglei

doi:10.3390/cancers14143377

Cited by 16 publications

(11 citation statements)

References 228 publications

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“…Integrins typically occur on the surface of cell membranes only for a limited period of time [ 13 ]. The presence or absence of integrins has a huge influence on the capacity of malignant tumours to invade and destroy local tissue, thus also on the metastasis of tumour cells [ 14 ]. A key factor in the carcinogenesis of pancreatic carcinoma is the family of NFAT (nuclear factor of activated T-cells) transcription factors [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of Ketamine, S-Ketamine and MK 801 on Integrin Beta-3-mediated Cell Migration in Pancreatic Carcinoma

Malsy¹,

Hofer²,

Schmidbauer³

et al. 2022

J Cancer Sci Clin Ther

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Introduction: Pancreatic ductal adenocarcinoma is one of the most aggressive malignancies in humans. The main reason for its unfavourable prognosis is the combination of rapid tumour growth, early-onset metastasis and currently still inadequate diagnostic and therapeutic options. Thus, only very few patients are eligible for radical resection of the primary tumour as the only curative treatment option available so far. In the perioperative period, tumour progression and metastasis are facilitated by the activation of key signalling pathways and the altered regulation of transcription factors. Various tumour entities have shown increased expression of the integrin-3 receptor subunit, which correlates with more rapid tumour progression and metastasis through advanced migration, invasion and proliferation. The influence of perioperative medication and postoperative pain management remains unclear. To investigate the effects of ketamine, s-ketamine and MK 801 on integrin beta-3-mediated cell migration in pancreatic cancer cells in vitro . Methods: The effects of ketamine, s-ketamine and MK 801 on integrin beta-3 expression were investigated with immunoblot. Cell migratory potentials were analysed using a Cell Migration Assay Kit with a Boyden chamber, in which cells migrate through a semipermeable membrane under different stimuli. Results: Stimulation with ketamine and MK 801 significantly promoted migration in pancreatic cancer cells, increasing the expression of integrin beta-3. Conclusion: Novel therapeutic approaches target the effective modulation of specific signalling and transcription pathways. The prerequisite for such ‘target therapies’ is comprehensive knowledge about the respective carcinogenesis. Further studies are required to identify the underlying disease mechanisms of pancreatic carcinoma.

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Section: Discussionmentioning

confidence: 99%

Effects of Ketamine, S-Ketamine and MK 801 on Integrin Beta-3-mediated Cell Migration in Pancreatic Carcinoma

Malsy¹,

Hofer²,

Schmidbauer³

et al. 2022

J Cancer Sci Clin Ther

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“…However, reports have shown that pancreatic adenocarcinoma remains refractory to conventional chemotherapeutics primarily because of the disease’s genetic heterogeneity and dense stroma, which inhibits penetration and accumulation of chemotherapeutics at the tumor sites. Hence, to improve the efficiency of pancreatic cancer therapy, selective penetration and accumulation of cytotoxic agents must be enhanced [ 19 , 35 , 110 ].…”

Section: Recent Advances In Pancreatic Cancer Targeted Therapy and Li...mentioning

confidence: 99%

“…Endoscopic ultrasound is also widely used in diagnosis in conjunction with other diagnostic techniques due to its ability to detect microscopic lesions [ 34 ]. However, early detection in patients does not automatically translate into reduced mortality; <35% of patients eligible for surgical intervention have a five-year rate of survival and approximately 85% of patients will experience a recurrence two years after surgery [ 11 , 16 , 18 , 34 , 35 , 36 ].…”

Section: Introductionmentioning

confidence: 99%

Drug Delivery Strategies for the Treatment of Pancreatic Cancer

et al. 2023

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Pancreatic cancer is fast becoming a global menace and it is projected to be the second leading cause of cancer-related death by 2030. Pancreatic adenocarcinomas, which develop in the pancreas’ exocrine region, are the predominant type of pancreatic cancer, representing about 95% of total pancreatic tumors. The malignancy progresses asymptomatically, making early diagnosis difficult. It is characterized by excessive production of fibrotic stroma known as desmoplasia, which aids tumor growth and metastatic spread by remodeling the extracellular matrix and releasing tumor growth factors. For decades, immense efforts have been harnessed toward developing more effective drug delivery systems for pancreatic cancer treatment leveraging nanotechnology, immunotherapy, drug conjugates, and combinations of these approaches. However, despite the reported preclinical success of these approaches, no substantial progress has been made clinically and the prognosis for pancreatic cancer is worsening. This review provides insights into challenges associated with the delivery of therapeutics for pancreatic cancer treatment and discusses drug delivery strategies to minimize adverse effects associated with current chemotherapy options and to improve the efficiency of drug treatment.

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“…Mainly early diagnosis of pancreatic cancer is difficult, and most patients are already in the late stage when diagnosed and cannot undergo surgical resection [3] . Understanding how pancreatic cancer starts and progresses, and discovering new treatments and drugs, can help patients with pancreatic cancer live longer and better [4] . Epidermal Growth Factor Receptor (EGFR) is a receptor that adds phosphate groups to tyrosine residues and regulates many cell processes, such as growth, movement, invasion, and death [5] .…”

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confidence: 99%

Effects of Erlotinib on Epidermal Growth Factor Receptor Signaling Pathway in Pancreatic Cancer Cells

Liu,

Zhou,

Lin

et al. 2024

IJPS

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Short Communication Liu et al.: Effects of Erlotinib on Pancreatic Cancer CellsThe number of people who get and die from pancreatic cancer, a deadly type of tumor, has been rising lately. Epidermal growth factor receptor is a receptor that adds phosphate groups to tyrosine residues and regulates many cell processes, such as growth, movement, invasion, and death. Pancreatic cancer cells have more epidermal growth factor receptor than normal cells, and this affects how they develop and survive. Erlotinib is a drug that blocks epidermal growth factor receptor activity and can treat some lung cancers with epidermal growth factor receptor mutations. The way erlotinib works against pancreatic cancer is still unknown. This research examines the impact of erlotinib on the proliferation and apoptosis of three types of pancreatic cancer cells; PANC-1, BxPC-3, and SW1990. The experiments used the 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide assay, Annexin V-fluorescein isothiocyanate/propidium iodide staining, quantitative reverse transcription-polymerase chain reaction, and enzyme-linked immunosorbent assay. Erlotinib can stop pancreatic cancer cells from growing, make them die, and lower the levels and activity of epidermal growth factor receptor and other molecules that send signals from it. This means that erlotinib could fight pancreatic cancer by blocking the epidermal growth factor receptor pathway, and offer a new way to treat it.

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Integrin β1 in Pancreatic Cancer: Expressions, Functions, and Clinical Implications

Cited by 16 publications

References 228 publications

Effects of Ketamine, S-Ketamine and MK 801 on Integrin Beta-3-mediated Cell Migration in Pancreatic Carcinoma

Effects of Ketamine, S-Ketamine and MK 801 on Integrin Beta-3-mediated Cell Migration in Pancreatic Carcinoma

Drug Delivery Strategies for the Treatment of Pancreatic Cancer

Effects of Erlotinib on Epidermal Growth Factor Receptor Signaling Pathway in Pancreatic Cancer Cells

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