LINC00173 (Long Intergenic Non-Protein Coding RNA 173)

LINC00173 can impair the malignancy of EC cell by interacting with HNRNPC. This finding may contribute to the understanding of the tumorigenic effects of HNRNPC and LINC00173 on EC.

Distinct functional disparities between estrogen subtypes emerge, with estradiol synergistically promoting ER+ BC cell growth with LINC00173, while estrone (E1) facilitated LITAF-transcriptional activation. In terms of therapeutic significance, silencing LINC00173 alongside moderate addition of E1 heightened TNFα and induced apoptosis, effectively inhibiting ER+ BC progression.

Taken together, we propose that LINC00173 positively regulates FHIT gene expression by binding to SNAIL and inhibiting its function in human lung adenocarcinoma. Thus, this study sheds light on the LINC00173-SNAIL-FHIT axis, which may be a key mechanism for carcinogenesis and progression in human lung adenocarcinoma.

LINC00173 functions as an oncogenic factor by binding with miR-765 to promote the progression of NPC via GREM1 upregulation. This study provides a novel insight into the molecular mechanisms involved in NPC progression.

Mechanistically, LINC00173 bound with checkpoint kinase 2 (CHK2) in nucleus, and impaired the irradiation-induced CHK2 phosphorylation, then suppressed the activation of P53 signalling pathway, which eventually inhibiting apoptosis and leading to radioresistance in NPC cells. In summary, LINC00173 decreases the occurrence of apoptosis through inhibiting the CHK2/P53 pathway, leads to NPC radioresistance and could be considered as a novel predictor and therapeutic target in NPC.

miR-218/Etk, miR-511-5p/VEGFA, miR-182-5p/AGER, miR-765/NUTF2, miR-765/PLP2, miR-182-5p/FBXW7, miR-338-3p/Rab25, miR‑641/RAB14 and miR-1275/BCL2 are examples of the miRNA/mRNA axes being regulated by LINC00173 in the context of cancer. The current review provides a summary of different studies on the role of LINC00173 in these cancers.

Nine studies involving 1102 patients were included.Meta-analysis showed that the overexpression of Linc00173 was significantly associated with poorer OS (HR = 1.76,95%CI:1.36-2.26, P < 0.001) and shorter DFS (HR = 1.89, 95%CI:1.49-2.40,P < 0.001),and was significantly associated with gender (male) (OR = 1.31,95% CI:1.01-1.69, P = 0.042), tumor size (large) (OR = 1.34,95% CI:1.01-1.78, P = 0.045), and lymph node metastasis (positive) (OR = 1.72,95% CI:1.03-2.88, P = 0.038). Overexpression of Linc00173 is associated with poor prognosis in cancer patients and is a potential prognostic biomarker and therapeutic target.

Moreover, in vivo LINC00173-knockdown models exhibited a marked slowdown in tumor growth, and a significant reduction in lymph node and lung metastases. In summary, LINC00173 serves as a crucial driver for NPC progression, and the LINC00173-RAB1B-PA2G4/SDF4 axis might provide potential therapeutic targets for NPC patients.

This work demonstrates that LINC00173 blocks GATA6-mediated transcription of COL5A1 to affect malignant development of OSCC.