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LncRNA LGALS8-AS1 Promotes Breast Cancer Metastasis Through miR-125b-5p/SOX12 Feedback Regulatory Network. | LitMetric

AI Article Synopsis

  • The long non-coding RNA LGALS8-AS1 is found to be highly expressed in breast cancer, correlating with poor patient survival and promoting tumor metastasis.
  • LGALS8-AS1 acts as an oncogene by upregulating SOX12 through its role as a competing endogenous RNA (ceRNA), which sponges miR-125b-5p and activates the PI3K/AKT signaling pathway to enhance cancer spread.
  • The study suggests that the reciprocal regulatory loop between LGALS8-AS1, miR-125b-5p, and SOX12 could be useful for developing new treatment strategies for breast cancer.

Article Abstract

Background: Metastasis is a major factor weakening the long-term survival of breast cancer patients. Increasing evidence revealed that long non-coding RNAs (lncRNAs) were involved in the occurrence and development of breast cancer. In this study, we aimed to investigate the role of LGALS8-AS1 in the metastatic progression of breast cancer cells and its potential mechanisms.

Results: The lncRNA LGALS8-AS1 was highly expressed in breast cancer and associated with poor survival. LGALS8-AS1 functioned as an oncogenic lncRNA that promoted the metastasis of breast cancer both and . It upregulated SOX12 competing as a competing endogenous RNA (ceRNA) for sponging miR-125b-5p and acted on the PI3K/AKT signaling pathway to promote the metastasis of breast cancer. Furthermore, SOX12, in turn, activated LGALS8-AS1 expression direct recognition of its sequence binding enrichment motif on the LGALS8-AS1 promoter, thereby forming a positive feedback regulatory loop.

Conclusion: This study manifested a novel mechanism of LGALS8-AS1 facilitating the metastasis of breast cancer. The LGALS8-AS1/miR-125b-5p/SOX12 reciprocal regulatory loop dyscrasia promoted the migration and invasion of breast cancer cells. This signaling axis could be applicable to the design of novel therapeutic strategies against this malignancy.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8570098PMC
http://dx.doi.org/10.3389/fonc.2021.711684DOI Listing

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