Int J Med Sci
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The cluster of differentiation 34 (CD34) family, which includes CD34, podocalyxin-like protein 1 (PODXL), and PODXL2, are type-I transmembrane sialomucins and markers of hematopoietic stem cells (HSCs) and vascular-associated tissues. CD34 family proteins are expressed by endothelial cells and hematopoietic precursors. PODXL is well known to be associated with invadopodia formation and to promote the epithelial-mesenchymal transition, tumor migration and invasion. ⋯ In a validation experiment, knockdown of PODXL2 in BT474 cells slightly influenced cell proliferation, suppressed migration, and inhibited expressions of downstream molecules, including Ras-related C3 botulinum toxin substrate 1 (Rac1), phosphorylated (p)-Akt (S473), and p-paxillin (Y31) proteins. In addition, knockdown of PODXL2 reduced expression levels of cancer stem cell (CSC) markers, including Oct-4 and Nanog, and the breast CSC marker aldehyde dehydrogenase 1 (ALDH1). Collectively, our present study demonstrated that PODXL2 plays a crucial role in cancer development and could serve as a potential prognostic biomarker in breast cancer patients.
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Treatment of advanced hepatocellular carcinoma (HCC) has exhibited a poor overall survival rate of only six to ten months, and the urgency of the development of more effective novel agents is ever present. In this line of research, we aimed to investigate the effects and inhibitive mechanisms of aqueous Ocimum gratissimum leaf extract (OGE), the extract of Ocimum gratissimum, which is commonly used as a therapeutic herb for its numerous pharmacological properties, on malignant HCC cells. Our results showed that OGE decreased the cell viability of HCC SK-Hep1 and HA22T cells in a dose-dependent manner (from 400 to 800 µg/mL), while there is little effect on Chang liver cells. ⋯ These findings raise suspicion that the OGE-induced cell death may be mediated through proteins that regulate cell cycle and apoptosis in SK-Hep1 and HA22T cells, and further experimentation revealed that OGE treatment resulted in a dose-dependent decrease in caspase 3 and PARP expressions and in CDK4and p-ERK1/2expressions. Moreover, animal tests also exhibited decreased HCC tumor growth by OGE treatment. We therefore suggest that the inhibition of cell viability and tumor growth induced by OGE may be correlated to the alteration of apoptosis-related proteins.
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Aspirin has been used as anti-inflammatory and anti-aggregate for decades but the precise mechanism(s) of action after the presence of the toxic peptide Aβ1-42 in cultured astrocytes remains poorly resolved. Here we use low-doses of aspirin (10-7 M) in astrocytes in primary culture in presence or absence of Aβ1-42 toxic peptide. We noted an increase of cell viability and proliferation with or without Aβ1-42 peptide presence in aspirin treated cells. ⋯ Aspirin inhibited COX-2 and iNOS without changes in COX-1 expression, increasing anti-oxidant protein (Cu/Zn-SOD and Mn-SOD) expression in presence or absence of Aβ1-42. Taken together, our results show that aspirin, at low doses increases cell viability by decreasing inflammation and oxidative stress, preventing the deleterious effects of the Aβ1-42 peptide on astrocytes in primary culture. The use of low doses of aspirin may be more suitable for Alzheimer's disease.
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Background: Fidgetin (FIGN), a conserved ATP-dependent enzyme, is regarded as a hepatocellular carcinoma (HCC) risk gene, but the prognostic implication of FIGN in HCC remains obscure. In this study, we investigate the expression of FIGN in HCC and to evaluate its prognostic value. Methods: A total of 216 patients with HCC who experienced hepatectomy were recruited in this study. ⋯ High expression of FIGN indicated shorter overall survival (OS) (hazard ratio: 4.569, P = 0.036) and disease-free survival (DFS) (hazard ratio: 6.487, P = 0.001). Conclusion: Our results indicate that high Fidgetin expression is associated with tumor progression and suggest a worse prognosis in HCC. Fidgetin might serve as a potential target for therapy.
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Evidence shows that long noncoding RNAs (lncRNAs) play key roles in various cancers, including colorectal cancer. In this current study, we found that the expression of ZEB1-AS1 in colorectal cancer tissues and cell lines was significantly upregulated, and positively correlated with advanced stage of colorectal cancer. Kaplan-Meier assays also indicated that the expression of ZEB1-AS1 was correlated with poor prognosis in patients with colorectal cancer. ⋯ The results of luciferase reporter assay proved that miR-141-3p was a target of ZEB1-AS1. Functionally, miR-141-3p inhibitor reversed the anti-proliferation effect of sh-ZEB1-AS1 on colorectal cancer cells. Collectively, ZEB1-AS1 may contribute to colorectal cancer cell proliferation by sponging miR-141-3p.