Related Experiment Video
Updated: Jan 30, 2026

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer
Published on: February 9, 2024
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.
Abstract:
The abnormal expression of long noncoding RNAs (lncRNAs) is closely associated with human cancers. As one special group of lncRNAs, natural antisense transcripts (NATs) can be transcribed from both DNA strands at the same locus but in the opposite direction from the gene transcript. Their expression levels are altered in many cancers, but their roles are poorly understood. We strove to find NATs involved in human non-small-cell lung cancer (NSCLC) and to reveal their mechanism of action in cancer. We analysed the NATs in NSCLC from the TCGA database by circlncRNAnet. One NAT, family with sequence similarity 83 member A antisense RNA 1 (FAM83A-AS1), was found to be markedly upregulated and positively correlated with its cognate sense counterpart, FAM83A, in NSCLC. Moreover, overexpression of FAM83A-AS1 increased FAM38A protein levels and induced ERK1/2 phosphorylation downstream of FAM83A in cells. Finally, overexpression of FAM83A-AS1 promoted LUAD cell proliferation and invasion. In summary, lncRNA FAM83A-AS1 promotes LUAD by increasing FAM83A expression.
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.
Related Concept Videos
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
The Eukaryotic Promoter Region
Bacterial RNA Polymerase
In most genes, the transcription site is a single base present upstream of the coding sequence. Though RNAP is a catalytically efficient enzyme, it does not recognize...
Eukaryotic RNA Polymerases
All three eukaryotic RNAPs require specific transcription factors, of which the...
Increasing Function
Lung Capacity

