These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: RP11-462C24.1 suppresses proliferation and invasion of colorectal carcinoma cells by regulating HSP70 through PI3K/AKT signaling pathway.
    Author: Zhang H, Zhang G, Liu H, Shan Y, Zhang X.
    Journal: Hum Cell; 2021 Jan; 34(1):132-151. PubMed ID: 32946066.
    Abstract:
    Colorectal cancer (CRC) is the third leading cause of cancer-related death around the world. In this study, we investigated the roles of LncRNA RP11-462C24.1 in CRC. The expressions of RP11-462C24.1 in CRC tissues and cells were measured. Then, the effects of RP11-462C24.1 on CRC proliferation, cell cycle, apoptosis, and invasion were evaluated both in vivo and in vitro; Last, the underlying mechanisms of concerning the signaling pathway regulated by RP11-462C24.1 was determined. From the results, we found that RP11-462C24.1 was significantly decreased in CRC tumor tissues and the CRC cell lines, which were most significant in SW480 and HT-29 cell lines; moreover, transient overexpression of RP11-462C24.1 suppressed the growth and migration while promoted apoptosis of SW480 and HT-29 cells, while knockdown of RP11-462C24.1 has shown the opposite effects; RP11-462C24.1 may also inhibit the growth of CRC tumors in xenograft mice models; additionally, 70 kD heat shock proteins (HSP70) has been identified as one of the most significantly deferentially expressed genes by RNA-seq, and we further confirmed that RP11-462C24.1 may affect the growth and metathesis of CRC cells via regulating HSP70 and PI3K/AKT signaling pathway. In summary, these results indicated that RP11-462C24 may function as a tumor suppressor in the development of CRC.
    [Abstract] [Full Text] [Related] [New Search]