Background Quercetin, a widely distributed bioflavonoid, plays a role in combating diverse human cancers including non‐small cell lung cancer (NSCLC). However, the role of quercetin in reversing the radioresistance of NSCLC cells and its underlying mechanism are far from being elucidated. Method Radiation‐resistant NSCLC cell lines were established. Quantitative real‐time PCR (qRT‐PCR) was used to detect the expression of miR‐16‐5p and WEE1 G2 checkpoint kinase (WEE1) mRNA in radiation‐resistant cells. After being treated with different concentrations of quercetin and different doses of X‐ray, cell proliferation and apoptosis were monitored by CCK‐8 assay, colony formation assay, and flow cytometry, respectively. Ultimately, the targeting relationship between miR‐16‐5p and WEE1 was verified via a dual fluorescent reporter gene assay. Results The expression of miR‐16‐5p was down‐regulated in radiation‐resistant cells, while the expression of WEE1 was up‐regulated. Quercetin enhanced the radiosensitivity of NSCLC cells in a dose‐ and time‐dependent manner. Furthermore, quercetin treatment increased the expression of miR‐16‐5p and decreased the expression of WEE1. The function of quercetin was reversed by miR‐16‐5p inhibitors or the transfection of WEE1 overexpressing plasmids. Conclusion In conclusion, quercetin enhanced the radiosensitivity of NSCLC cells via modulating the expression of miR‐16‐5p and WEE1.
Previous studies have revealed that HURP (also known as DLGAP5 or KIAA0008) is overexpressed in many types of human cancers, such as hepatocellular carcinoma, squamous cell bladder cancer, and transitional cell carcinoma, indicating that HURP is a putative oncoprotein that promotes carcinogenesis through various molecular mechanisms. However, the role of HURP in the pathogenesis of non-small cell lung cancer (NSCLC) has not been reported. In the present study, we investigated the prognostic value of HURP among NSCLC patients through the GEO database. The online tool of KM-plotter was used to identify the correlation of HURP expression and the survival of NSCLC patients. We found the HURP expression at the mRNA level was correlated with the clinicopathologic characteristics and prognosis of NSCLC patients. HURP was highly expressed in aggressive NSCLC cells, and its higher expression was associated with shorter survival. Further cytological experiments revealed that the silencing of HURP caused cell cycle arrest and inhibited the proliferation of NSCLC cells. Transwell assay showed that HURP shRNA inhibited cell migration and invasion in vitro. The bioinformatic analysis suggests that HURP promotes carcinogenesis in multiple manners. Taken together, we revealed the prognostic value of HURP in NSCLC patients and HURP may be a potential therapeutic target for NSCLC.
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can selectively induce apoptosis of cancer cells and is verified effective to various cancers. However, a variety of breast cancer cell lines are resistant to TRAIL and the mechanisms of resistance are largely unknown. In our present experiment, we successfully utilized breast cancer cell line MDA-MB-231 to establish TRAIL-resistant cell line. We found resistance to TRAIL could induce epithelial-mesenchymal transition (EMT) and enhance invasiveness. We further demonstrated PTEN was down-regulated in TRAIL-resistant cells. Silencing miR-221, PTEN expression was up-regulated, the process of EMT could be reversed, and the ability of migration and invasion were correspondingly weakened. We also demonstrated knockdown of miR-221 could reverse resistance to TRAIL partially by targeting PTEN. Our findings suggest that resistance to TRAIL could induce EMT and enhance invasiveness by suppressing PTEN via miR-221. Re-expression of miR-221 or targeting PTEN might serve as potential therapeutic approaches for the treatment of Trail-resistant breast cancer.
Background: About 70% of human breast cancers express estrogen receptor α (ERα) and in this kind of breast cancer estrogen plays an important role. Estrogen independent growth has been reported to promote resistance to one of the selective estrogen receptor modulators (SERMs) tamoxifen which is clinically the first line treatment for patients with ERα-positive breast cancer. The resistance of tamoxifen is a major problem in the clinical management of breast cancer. Methods: We used MCF-7 cells with ectopic expression of MDTH in this study. MTT, clone formation and tumor formation in nude mice methods were utilized to confirm the role of MTDH in estrogen-independent growth and tamoxifen resistance. Flow cytometry, western blot and siRNA were used to study the detailed mechanisms. Results: We found that MTDH could mediate estrogen-independent growth and induce resistance to tamoxifen in ERα-positive breast cancer cells. MTDH could reduce the expression of PTEN, up-regulate AKT and BCL2 and inhibit the apoptosis induced by tamoxifen. Conclusion: Our study indicated that MTDH was a candidate marker to predict the clinical efficacy of tamoxifen and targeting MTDH would overcome the resistance to tamoxifen in breast cancer cells.
Direct visualization evidence is important for understanding the microbial degradation mechanisms. To track the microbial degradation pathways of azo dyes with different polar characterizations, sensors based on the fluorescence resonance energy transfer (FRET) from 1,8-naphthalimide to azo dyes were synthesized, in which the quenched fluorescence will recover when the azo bond was cleaved. In living cells, the sensor-tracking experiment showed that the low polarity and hydrophobic azo dye can be taken up into the cells and reduced inside the cells, whereas the high polarity and hydrophilic azo dye can be reduced only outside the cells because of the selective permeability of the cell membranes. These results indicated that there were two different bacterial degradation pathways available for different polarity azo dyes. To our knowledge, no fluorescent sensor has yet been designed for illuminating the microbial degradation mechanisms of organic pollutants with different characteristics.
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