Effect of 5-aminolevulinic acid on the haem biosynthesis pathway in pancreatic cancer and pancreatic ductal epithelial cell lines

AbstractBackground and aimThis investigation was aimed at disclosing whether SRPX2 affected pancreatic cancer (PC) chemoresistance by regulating PI3K/Akt/mTOR signaling.MethodsTotally 243 PC patients were recruited, and they were incorporated into partial remission (PR) group, stable disease (SD) group and progressive disease (PD) group in accordance with their chemotherapeutic response. PC cell lines (i.e. AsPC1, Capan2, VFPAC-1, HPAC, PANC-1, BxPC-3 and SW1990) and human pancreatic ductal epithelial cell lines (hTERT-HPNE) were also collected.ResultsPC patients of SD + PD group were associated with higher post-chemotherapeutic SRPX2 level than PR group, and their post-chemotherapeutic SRPX2 level was above the pretherapeutic SRPX2 level (P < 0.05). PR population showed lower SRPX2 level after chemotherapy than before chemotherapy (P < 0.05). Besides high serum SRPX2 level and SRPX2 level change before and after chemotherapy were independent predictors of poor PC prognosis. Additionally, si-SRPX2 enhanced chemosensitivity of PC cell lines, and expressions of p-PI3K, p-AKT and p-mTOR were suppressed by si-SRPX2 (P < 0.05). IGF-1 treatment could changeover the impact of si-SRPX2 on proliferation, migration, invasion and chemoresistance of PC cells (P < 0.05).ConclusionThe SRPX2-PI3K/AKT/mTOR axis could play a role in modifying progression and chemoresistance of PC cells, which might help to improve PC prognosis.

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Regulation of hTERT Expression and Function in Newly Immortalized p53 (+) Human Mammary Epithelial Cell Lines

10.21236/ada440296 ◽

2005 ◽

Author(s):

Martha R. Stampfer

Keyword(s):

Epithelial Cell ◽

Cell Lines ◽

Mammary Epithelial Cell ◽

Human Mammary Epithelial Cell ◽

Mammary Epithelial ◽

Htert Expression ◽

Epithelial Cell Lines ◽

Human Mammary Epithelial ◽

And Function

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Cationic amino acid transport by two renal epithelial cell lines: LLC-PK1and MDCK cells

Journal of Cellular Physiology ◽

10.1002/jcp.1041230121 ◽

1985 ◽

Vol 123 (1) ◽

pp. 144-150 ◽

Cited By ~ 20

Author(s):

Francisco V. Sepúlveda ◽

Jeremy D. Pearson

Keyword(s):

Amino Acid ◽

Epithelial Cell ◽

Cell Lines ◽

Amino Acid Transport ◽

Mdck Cells ◽

Acid Transport ◽

Renal Epithelial Cell ◽

Cationic Amino Acid ◽

Epithelial Cell Lines

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Essential Role of Visfatin in Lipopolysaccharide and Colon Ascendens Stent Peritonitis-Induced Acute Lung Injury

International Journal of Molecular Sciences ◽

10.3390/ijms20071678 ◽

2019 ◽

Vol 20 (7) ◽

pp. 1678 ◽

Cited By ~ 1

Author(s):

Yi-Chen Lee ◽

Chun-Yu Lin ◽

Yen-Hsu Chen ◽

Wen-Chin Chiu ◽

Yen-Yun Wang ◽

...

Keyword(s):

Acute Lung Injury ◽

Epithelial Cell ◽

Lung Injury ◽

Cell Lines ◽

Inflammatory Cytokines ◽

Bronchial Epithelial Cell ◽

Bronchial Epithelial ◽

Epithelial Cell Lines ◽

Nfκb Pathway ◽

Pro Inflammatory Cytokines

Acute lung injury (ALI) is a life-threatening syndrome characterized by acute and severe hypoxemic respiratory failure. Visfatin, which is known as an obesity-related cytokine with pro-inflammatory activities, plays a role in regulation of inflammatory cytokines. The mechanisms of ALI remain unclear in critically ill patients. Survival in ALI patients appear to be influenced by the stress generated by mechanical ventilation and by ALI-associated factors that initiate the inflammatory response. The objective for this study was to understand the mechanisms of how visfatin regulates inflammatory cytokines and promotes ALI. The expression of visfatin was evaluated in ALI patients and mouse sepsis models. Moreover, the underlying mechanisms were investigated using human bronchial epithelial cell lines, BEAS-2B and NL-20. An increase of serum visfatin was discovered in ALI patients compared to normal controls. Results from hematoxylin and eosin (H&E) and immunohistochemistry staining also showed that visfatin protein was upregulated in mouse sepsis models. Moreover, lipopolysaccharide (LPS) induced visfatin expression, activated the STAT3/NFκB pathway, and increased the expression of pro-inflammatory cytokines, including IL1-β, IL-6, and TNF-α in human bronchial epithelial cell lines NL-20 and BEAS-2B. Co-treatment of visfatin inhibitor FK866 reversed the activation of the STAT3/NFκB pathway and the increase of pro-inflammatory cytokines induced by LPS. Our study provides new evidence for the involvement of visfatin and down-stream events in acute lung injury. Further studies are required to confirm whether the anti-visfatin approaches can improve ALI patient survival by alleviating the pro-inflammatory process.

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