Unknown

Dataset Information

0

LncRNA MCF2L-AS1 aggravates the malignant development of colorectal cancer via targeting miR-105-5p/RAB22A axis.


ABSTRACT:

Background

Colorectal cancer (CRC) represents one of the major malignant cancers in the world. It has been demonstrated that long non-coding RNAs (lncRNAs) can cause great influences on various human cancers. Though MCF.2 cell line derived transforming sequence like antisense RNA 1 (MCF2L-AS1) and its carcinogenic effect in CRC has been elucidated by several previous researches, the underlying mechanism remains unknown.

Aim

We aimed at exploring the function and regulatory mechanism of MCF2L-AS1 in CRC.

Methods

MCF2L-AS1 expression in CRC cells was tested via RT-qPCR assay. The effects of MCF2L-AS1 on the biological properties of CRC cells were testified through functional experiments. The molecular mechanism of MCF2L-AS1 was verified through mechanism experiments.

Results

MCF2L-AS1 was highly expressed in CRC cells, and it could enhance the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) process of CRC cells. MiR-105-5p was sponged by MCF2L-AS1 in CRC cells and Ras-related protein Rab-22A (RAB22A) was verified to be the downstream target of miR-105-5p. It was verified through rescue assays that RAB22A overexpression or miR-105-5p silencing could reverse the repressive impact of MCF2L-AS1 silencing on CRC progression.

Conclusion

MCF2L-AS1 accelerated the malignant development of CRC cells by targeting the miR-105-5p/RAB22A axis.

SUBMITTER: Kong W 

PROVIDER: S-EPMC8482615 | biostudies-literature |

REPOSITORIES: biostudies-literature

Similar Datasets

| S-EPMC10373981 | biostudies-literature
| S-EPMC9279048 | biostudies-literature
| S-EPMC10259264 | biostudies-literature
| S-EPMC10676586 | biostudies-literature
| S-EPMC7417701 | biostudies-literature
| S-EPMC8596928 | biostudies-literature
| S-EPMC8966157 | biostudies-literature
| S-EPMC8464591 | biostudies-literature
| S-EPMC7373409 | biostudies-literature
| S-EPMC8072314 | biostudies-literature