Target intelligence / Profile preview

Family with sequence similarity 99 member A (non-protein coding) (FAM99A)

Target
FAM99A
Molecular classification
Long non-coding RNA (lncRNA), Other
01

Overview

Family with sequence similarity 99 member A (FAM99A) is a liver-specific long non-coding RNA (lncRNA), predominantly localized in the nuclei of liver cells[2]. FAM99A acts as a tumor suppressor in hepatocellular carcinoma (HCC), with lower expression linked to poor prognosis and aggressive clinical features[2][3]. Functionally, FAM99A inhibits HCC cell proliferation, migration, invasion, glycolysis, and epithelial-mesenchymal transition (EMT) by regulating key pathways including JAK2/STAT3 and by interacting with RNA binding proteins such as EIF4B, PCBP1, and others[1][2][4]. Overexpression of FAM99A suppresses tumor growth in vivo in animal models[1][2]. FAM99A is not itself a therapeutic target in the traditional sense (i.e., it is not a receptor, enzyme, or transporter), but may be relevant as a biomarker for prognosis and potentially as a mediator targeted indirectly by small molecule therapeutics, such as icaritin, that modulate lncRNA expression[1][2].

Other names
FLJ42833family with sequence similarity 99 member AFAM99A (non-protein coding)lncRNA FAM99A
02

Mechanism of action

Icaritin-induced upregulation of FAM99A leads to inhibition of GLUT1-mediated glycolysis through inactivation of the JAK2/STAT3 pathway[1]

03

Biological functions

Regulation of glycolysis via JAK2/STAT3 signaling pathway[1]Suppression of cell proliferation and clonogenicity in hepatocellular carcinoma (HCC) cells[2]Inhibition of cell migration and invasion (in HCC)[2]Inhibition of epithelial-mesenchymal transition (EMT)[4]Regulation of gene expression through nuclear functions and interaction with RNA-binding proteins[2]Potential involvement in chromatin organization and transcriptional/post-transcriptional regulation[2]
04

Disease associations

Cancer (primarily Liver cancer/Hepatocellular carcinoma)[2][1][3]Prognostic biomarker in HCC[2]Possible involvement in tumor microenvironment and immune escape[1]Other
05

Safety considerations

None reported in current literature; as a non-coding RNA, direct therapeutic targeting safety concerns are under-investigated[1][2]
06

Interacting drugs

Icaritin (shown to induce FAM99A and inhibit glycolysis in HCC models)[1]
07

Biomarkers

FAM99A expression as a prognostic biomarker for HCC patient survival and progression[2]GLUT1 expression (downregulated upon FAM99A upregulation)[1]Possibly SOCS3 and miR-299-5p levels in tumor tissues[1]

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