Rabbit Anti-Human MAPKAPK2 (internal) Polyclonal antibody

Reticulon-4 (RTN4), a reticulon family protein localized in the endoplasmic reticulum, is reported to be involved in multiple physiological processes like neuroendocrine secretion and membrane trafficking in neuroendocrine cells. Previous studies have presented a great potential of RTN4 for the treatment of autoimmune-mediated demyelinating diseases and spinal cord injury regeneration. While interaction with Bcl-2 and Bcl-2-like family in apoptosis modulation implicated its possible role in various human cancers. However, the investigation of this gene in prostate cancer is mainly ignored. Here in our current study, we focused on its role in prostate cancer and found that RTN4 DNA copy numbers were higher in prostate cancer than normal prostate gland while its RNA and protein expressions were relatively lower. Chromosomal neighbor gene EML6 had similar expression patterns with RTN4 in prostate cancer tissues and cell lines, and further research found that they could be both targeted by miR-148a-3p. Lentivirus-mediated RTN4 overexpression potently inhibited DU145 and LNCaP cells proliferation. Cell cycle was blocked in G2/M phase and significant cell senescence was observed in RTN4 overexpressed prostate cancer cells. Finally, interaction networks in the normal prostate gland and cancer tissues further revealed that RTN4 maybe phosphorylated by MAPKAPK2 and FYN at tyrosine 591 and serine 107, respectively. All these results implied that RTN4 might somehow participate in prostate tumor progression, and this elicits possibility to develop or identify selective agents targeting RTN4 for prostate cancer therapy.

Colon cancer is the third most common malignancy in the world. Long-chain noncoding RNA urothelial carcinoma-associated 1 (UCA1) was abnormally expressed in colon cancer and participated in colon cancer by regulating multiple miRNAs. This study further explored the molecular mechanism of UCA1 in the development of colon cancer from both in vitro and in vivo. The results showed that UCA1 was highly expressed in colon cancer cells, while miR-185-5p was low expressed. Bioinformatics analysis showed that miR-185-5p was a target of UCA1, while MAPK14 was a target of miR-185-5p. Knockdown of UCA1 with shRNA (sh-UCA1) resulted in a significant increase in miR-185-5p and a significant decrease in MAPK14. In addition, sh-UCA1 inhibited invasion, migration and epithelial-mesenchymal transformation of colon cancer cells. Western blotting also showed that sh-UCA1 inactivated the MAPKAPK2/HSP27 pathway. Furthermore, animal studies have revealed that sh-UCA1 inhibited tumour formation in vivo and improved the survival rate of mice. Collectively, these results suggest that silencing UCA1 may inhibit the carcinogenesis and metastasis of colon cancer in vitro and in vivo by modulating miR-185-5p/MAPK14/MAPKAPK2/HSP27 axis. Significance of the study Colon cancer is the third largest malignant tumour worldwide. This study elucidated the role of urothelial carcinoma-associated 1 (UCA1) in colon cancer cells and its molecular mechanism. The present study suggests that silencing UCA1 may inhibit the invasion, migration, epithelial-mesenchymal transformation and tumour formation of colon cancer by upregulating miR-185-5p in vitro and in vivo. In summary, this study provides a new strategy for targeted therapy of colon cancer.