ABSTRACT
Colon cancer is one of the most common digestive tumors. The present study aimed to explore the functional role, as well as the underlying mechanism of long non-coding RNA LINC00261 in colon cancer. Expression of LINC00261 was analyzed in colon cancer cell lines and human normal cell lines. Acquired resistance cell lines were then built and the acquired resistance efficiency was detected by evaluating cell viability. Thereafter, the effects of LINC00261 overexpression on cisplatin-resistant colon cancer cells were measured, as well as cell apoptosis, viability, migration, and invasion. Subsequently, we investigated the interaction of LINC00261 and β-catenin. The results showed that the LINC00261 gene was down-regulated in colon cancer cell lines and tissues, and in cisplatin-resistant cells. LINC00261 overexpression might relieve cisplatin resistance of colon cancer cells via promoting cell apoptosis, and inhibiting cell viability, migration, and invasion. Moreover, LINC00261 might down-regulate nuclear β-catenin through restraining β-catenin from cytoplasm into nuclei or it could also promote β-catenin degradation and inhibit activation of Wnt pathway. Finally, LINC00261 reduced cisplatin resistance of colon cancer in vivo and enhanced the anti-colon cancer effect of cisplatin through reducing tumor volume and weight.
Subject(s)
Humans , RNA, Long Noncoding/physiology , Antineoplastic Agents/pharmacology , Tetrazolium Salts , Thiazoles , Down-Regulation , Blotting, Western , Reproducibility of Results , Analysis of Variance , Apoptosis/drug effects , Apoptosis/physiology , Apoptosis Regulatory Proteins/drug effects , beta Catenin/physiology , Cell Migration AssaysABSTRACT
We report a case of a 76-year old female presenting with symptomatic severe hypercalcaemia, and subsequently diagnosed with late onset SLE due to the presence of anaemia, leucopenia, antibodies of antinuclear (ANA), anti-dsDNA, and also kidney impairment. Serum levels of FGF23 and intact-parathyroid hormone (iPTH) were low in this patient. Serum calcium, FGF23 and iPTH levels responded to steroids, which occurred simultaneously with disease activity. On follow-up, the faster increase in FGF23 than in parathyroid hormone suggested that FGF23 might be involved in the pathogenesis of hypercalcaemia in SLE.
Se reporta el caso de una mujer de 76 años de edad que se presentó con hipercalcemia sintomática severa, y a la que posteriormente le fuera diagnosticada LES de inicio tardío con presencia de anemia, leucopenia, anticuerpos antinucleares (ANA), anti-dsDNA, e insuficiencia del riñón. Los niveles séricos del factor de crecimiento fibroblástico 23 (FGF23) y la hormona paratiroidea intacta (iPTH) fueron bajos en este paciente. Los niveles de calcio séricos, FGF23 e iPTH respondieron a los esteroides, que ocurrieron simultáneamente con la actividad de la enfermedad. En el seguimiento, el hecho de que el factor FGF23 aumentara más rápidamente que la hormona paratiroidea, sugiere que el FGF23 podría estar involucrado en la patogénesis de la hipercalcemia en LES.