Target intelligence / Profile preview

MicroRNA let-7g (MIRLET7G)

Target
MIRLET7G
Molecular classification
MicroRNA, Non-coding RNA, Tumor suppressor (functional classification)
01

Overview

MicroRNA let-7g (MIRLET7G) is a highly conserved, small non-coding RNA that functions mainly as a tumor suppressor by regulating gene expression at the post-transcriptional level. It belongs to the let-7 family, one of the first-discovered and most studied microRNA families, playing a crucial role in controlling cell differentiation, proliferation, and developmental timing. MIRLET7G acts primarily by binding to complementary sequences in target mRNAs, leading to translational repression or mRNA degradation, with key targets including oncogenes such as MYC, RAS, and HMGA2. Dysregulation or reduced expression of let-7g contributes to tumorigenesis and is associated with poor clinical outcomes in various cancers. Therapeutic strategies are under exploration using let-7g mimics or inducers to restore its tumor suppressor function, although challenges remain regarding delivery, specificity, and safety[1][4][5][7].

Other names
LET7Glet-7gMIRNLET7Ghsa-let-7gMIRLET7G[1][7]
02

Mechanism of action

miRNA mimics: Increase let-7g activity to suppress oncogene expression. Antagomirs/inhibitors: Block let-7g, increasing expression of its targets. Indirect: Drugs affecting let-7g regulators (e.g., LIN28 inhibition increases let-7g levels).

03

Biological functions

Post-transcriptional regulation of gene expressionCell differentiationCell proliferation inhibitionTumor suppressionRegulation of mRNA stability and translationDevelopmental timingRegulation of apoptosis
04

Disease associations

Cancer (particularly as tumor suppressor, e.g., lung, gastric, colon cancer)Potential roles in inflammation and infection (notably viral infection regulation)Stem cell maintenance and reprogramming
05

Safety considerations

Systemic modulation may disrupt normal stem cell differentiation and developmentOff-target effects due to widespread gene regulation by let-7 familyPotential for affecting tissue regeneration and homeostasis if delivered broadly
06

Interacting drugs

None directly approved or established as interacting with MIRLET7G; however, nucleic acid-based therapeutics (e.g., let-7 mimics, antagomirs) and modulators of upstream regulators such as LIN28 are in preclinical/experimental stages.
07

Biomarkers

Low expression of let-7 family (including let-7g) is a prognostic biomarker in multiple cancers, especially lung carcinoma

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