Long non-coding RNA CRNDE may be associated with poor prognosis by promoting proliferation and inhibiting apoptosis of cervical cancer cells through targeting PI3K/AKT

Rok, strany: 2018, 872 - 880

Long non-coding RNAs (lncRNAs) are attracting more and more attention from researchers because they are relatively new factors in regulating biological processes in human cancers. The Colorectal Neoplasia Differentially Expressed (CRNDE) lncRNA is transcribed from chromosome 16 on the opposite strand to the neighboring IRX5 gene. It was originally discovered abnormally expressed in colorectal cancer (CRC) and was certified a critical biomarker in many cancers. However, its biological function and mechanism underlying the tumorigenesis of cervical cancer still require exploration. This study confirmed that CRNDE is markedly up-regulated in clinical tissues and cell lines of cervical cancer. The high expression of CRNDE positively correlates with advanced FIGO stage and lymph node metastasis. Furthermore, the overall survival rate in the group with highly expressed CRNDE was worse, and the high level of CRNDE may be regarded a prognostic factor because of its results from proportional hazard analysis. Loss-of-function assays revealed that CRNDE influences proliferation and apoptosis in cervical cancer cells, and Western blot assays revealed that the PI3K/AKT pathway was inactivated in response to CRNDE knockdown. Therefore, we conclude that CRNDE exerts oncogenic function in cervical cancer and should be further explored as a novel prognostic predictor.

ISO 690:

Yang, H., Huang, C., Cao, M., Wang, Y., Liu, Y. 2018. Long non-coding RNA CRNDE may be associated with poor prognosis by promoting proliferation and inhibiting apoptosis of cervical cancer cells through targeting PI3K/AKT. In NEOPLASMA, vol. 65, no.6, pp. 872-880. 0028-2685.

APA:

Yang, H., Huang, C., Cao, M., Wang, Y., Liu, Y. (2018). Long non-coding RNA CRNDE may be associated with poor prognosis by promoting proliferation and inhibiting apoptosis of cervical cancer cells through targeting PI3K/AKT. NEOPLASMA, 65(6), 872-880. 0028-2685.