Mitochondrial estrogen receptor β inhibits non-small cell lung cancer cell apoptosis via interaction with Bad / 南方医科大学学报

<p><b>OBJECTIVE</b>To explore the molecular mechanisms by which mitochondrial estrogen receptor β (ERβ) suppresses non-small cell lung cancer cell apoptosis induced by apoptotic stimulations.</p><p><b>METHODS</b>The mitochondrial localization of ERβ in non-small cell lung cancer cell lines A549 and 201T was determined using immunofluorescence and Western blotting. The changes of apoptosis of the cells with mitochondrial ERβ overexpression or knockdown in response to cisplatin and STS treatments were assessed, and mitochondrial ERβ interaction with the pro-apoptotic protein Bad was detected using co-immunoprecipitation and Western blotting.</p><p><b>RESULTS</b>ERβ was localized in the mitochondria in A549 and 201T cells. ERβ overexpression significantly reduced while ERβ knockdown increased Bax activation and cell apoptosis induced by cisplatin and STS. Mitochondrial ERβ interaction with pro-apoptotic protein Bad may suppress Bax activation and its translocation to the mitochondria.</p><p><b>CONCLUSION</b>Mitochondrial ERβ can suppress apoptosis of non-small cell lung cancer cells induced by cisplatin or STS through interaction with Bad, suggesting the value of mitochondrial ERβ as a new therapeutic target for treatment of non-small cell lung cancer.</p>

miR-221 mediates epithelial-mesenchymal transition-related gene expressions via regulation of PTEN/Akt signaling in drug-resistant glioma cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the correlation between miR-221 and epithelial-mesenchymal transition (EMT) in drug-resistant glioma cells.</p><p><b>METHODS</b>The expression levels of miR-221, PTEN, p-Akt, E-cadherin, vimentin, and MRP1 were quantitatively analyzed in Z1 cells (primary drug-resistant cells), Z2 cells (drug-sensitive cells) and Z2-BCNU cells (drug-resistant cells) using fluorescent real-time PCR and Western blotting.</p><p><b>RESULTS</b>The expression levels of PTEN were significantly increased in Z2 cells compared with Z1 and Z2-BCNU cells which overexpressed miR-221 and vimentin. The expression levels of vimentin, p-Akt and MRP1 were significantly decreased in Z2 cells overexpressing E-cadherin.</p><p><b>CONCLUSION</b>MiR-221 regulates the expression of EMT-related genes through down-regulation of PTEN and activation of PI3-K/Akt signaling.</p>

CD99 regulates redifferentiation of classical Hodgkin's lymphoma cell line L428 towards B cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To explore the effect of CD99 overexpression on the morphology and differentiation-related phenotypes of classical Hodgkin's lymphoma cell line L428 and investigate the role of CD99 gene in Hodgkin/Reed-Sternberg (HRS) cell generation and transformation.</p><p><b>METHODS</b>The effect of CD99 overexpression on the cell morphology was detected by HE staining and phalloidin staining. Differentiation-related protein expressions were detected by immunocytochemistry and flow cytometry after stable transfection of CD99 gene in L428 cells.</p><p><b>RESULTS</b>CD99 overexpression caused a decrease of the cell size and reorganization of the actin cytoskeleton in L428 cells. Upregulation of CD99 led to the loss of classical Hodgkin's lymphoma diagnosis marker CD30 and CD15 and the restoration of the B-cell makers of PAX5, CD19, CD79α, BCL-6, and CD10.</p><p><b>CONCLUSION</b>CD99 overexpression leads to redifferentiation of L428 cells towards B cells, suggesting that the loss of B-cell phenotype in classical Hodgkin's lymphoma is very likely a result of down-regulated CD99 expression.</p>