Long noncoding antisense RNA FAM83A-AS1 promotes lung cancer cell progression by increasing FAM83A

Rongxing Shi1, Zichen Jiao1,2, Ao Yu1

  • 1Department of Cardiothoracic Surgery, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing, China.

Insights

Long noncoding RNA (lncRNA) FAM83A-AS1 is upregulated in non-small cell lung cancer (NSCLC). This lncRNA promotes lung adenocarcinoma (LUAD) by increasing FAM83A expression, driving cell proliferation and invasion.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genomics

Background:

  • Abnormal long noncoding RNA (lncRNA) expression is linked to human cancers.
  • Natural antisense transcripts (NATs), a type of lncRNA, have altered expression in many cancers, but their roles remain unclear.

Purpose of the Study:

  • Identify NATs involved in non-small cell lung cancer (NSCLC).
  • Elucidate the mechanism of action for identified NATs in cancer progression.

Main Methods:

  • Analysis of NATs in NSCLC using The Cancer Genome Atlas (TCGA) database and circlncRNAnet.
  • Investigated the functional impact of FAM83A-AS1 overexpression on protein levels, signaling pathways, and cell behavior.

Main Results:

  • Identified FAM83A-AS1, a NAT, significantly upregulated in NSCLC and positively correlated with its sense counterpart, FAM83A.
  • Overexpression of FAM83A-AS1 increased FAM83A protein levels and ERK1/2 phosphorylation.
  • FAM83A-AS1 overexpression promoted lung adenocarcinoma (LUAD) cell proliferation and invasion.

Conclusions:

  • lncRNA FAM83A-AS1 acts as an oncogene in LUAD.
  • FAM83A-AS1 promotes LUAD progression by upregulating FAM83A expression and downstream signaling pathways.

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