ABSTRACT
OBJECTIVE@#To investigate the expression of LINC01106 in colorectal cancer and its role in regulating the proliferation and apoptosis of colorectal cancer cells.@*METHODS@#We analyzed the data of LINC01106 expression levels in tumor tissues and normal tissues of patients with colorectal cancer in TCGA database and explored the association of LINC01106 expression level with the prognosis of the patients. Colorectal cancer SW480 cell lines with LINC01106 knockdown or overexpression were established, and their proliferation and apoptosis relative to the parental cells were evaluated using CCK-8 assay and flow cytometry, respectively. The expressions of p-STAT3, STAT3, and Bcl-2 in the cells were detected by immunoblotting. Nude mouse models bearing xenografts of SW480 cells with LINC01106 knockdown or na?ve SW480 cells were established to observe the effect of LINC01106 knockdown on the growth of SW480 cells .@*RESULTS@#Analysis of the data from TCGA database showed that the expression level of LINC01106 was significantly higher in colorectal cancer tissues than in normal tissues, and LINC01106 expression level was significantly related to the prognosis of the patients ( < 0.05). Knockdown of LINC01106 significantly inhibited the proliferation and promoted apoptosis of SW480 cells ( < 0.05), while LINC01106 overexpression significantly promoted proliferation of the cells. LINC01106 knockdown in SW-480 cells obviously lowered the expressions of p- STAT3 and Bcl-2 and suppressed the growth of the xenograft in nude mice.@*CONCLUSIONS@#LINC01106 is significantly up-regulated in colorectal cancer tissue and is related to the prognosis of the patients. LINC01106 can regulate the proliferation and apoptosis of SW480 cells through STAT3/Bcl-2 signaling and may serve as a potential marker for the diagnosis and prognostic evaluation of colorectal cancer.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of Src kinase inhibitor PP2 on hypoxia/reoxygenation (H/R) injury in rat astrocytes in vitro.</p><p><b>METHODS</b>In vitro cultured rat astrocytes were exposed to hypoxia for 8 h followed by reoxygenation for 24 h with or without pretreatment with PP2 (10 µmol/L) for 24 h before H/R injury. MTT assay and flow cytometry were used to detect the viability and apoptosis of the exposed astrocytes, respectively, and the protein expressions of Src, Bax, and Bcl-2 in the cells were determined using Western blotting.</p><p><b>RESULTS</b>PP2 pretreatment significantly increased the viability and decreased the apoptosis rate of rat astrocytes exposed to H/R injury (P<0.01). Western blotting showed that H/R injury caused increased expression of Src kinase, which was lowered by PP2 pretreatment. The ratio of Bax/bcl-2 in the astrocytes increased after H/R injury, and was significantly decreased by PP2 pretreatment (P<0.01).</p><p><b>CONCLUSION</b>PP2 protects rat astrocytes from H/R injury possibly by inhibiting the expression of Src kinase and activating the anti-apoptotic mechanisms in the cells.</p>
Subject(s)
Animals , Rats , Apoptosis , Astrocytes , Pathology , Cell Hypoxia , Cells, Cultured , Flow Cytometry , Pyrimidines , Pharmacology , src-Family KinasesABSTRACT
<p><b>OBJECTIVE</b>To determine the expression of connexin 43 (Cx43) protein and explore the functional modulation of gap junction intercellular communication in astrocytes.</p><p><b>METHODS</b>Cultured neonatal SD rat astrocytes were divided into normal control group, all-trans retinoic acid (ATRA) group (treated with 10 µmol/L ATRA for 24 h) and oleamide group (treated with 25 µmol/L oleamide for 2 h). Western blotting and immunofluorescence assay were used to detect total cellular Cx43 protein expression and Cx43 expression on the surface of the astrocytes, respectively. Parachute assay was used to evaluate the functional changes of gap junction intercellular communication of the astrocytes.</p><p><b>RESULTS</b>Compared with the normal control cells, ATRA treatment resulted in a significantly increased expression of total Cx43 protein in the astrocytes (P<0.01), and oleamide significantly suppressed its expression (P<0.01). Similarly, ATRA obviously enhanced while oleamide suppressed Cx43 protein expression on the surface of the astrocytes. The gap junction intercellular communication of the astrocytes was enhanced by ATRA (P<0.01) and inhibited by oleamide (P<0.01).</p><p><b>CONCLUSION</b>ATRA and oleamide can modulate gap junction intercellular communication of the astrocytes possibly by regulating the expression of Cx43 protein.</p>