LINC00520 expression

LINC00520 functions as a modulator of calcium deposits, and exosomes derived from hucMSCs overexpressing LINC00520 might be a novel therapeutic approach for osteoporosis.

Finally, the rescuing experiments evidenced that both POSTN knockdown and ILK/Akt/mTOR pathway inhibitor OSU-T315 abrogated the promoting effects of miR-577 ablation on the malignant phenotypes in BC. Collectively, this study firstly verified that LINC00520 acted as a ceRNA of miR-577 to advance BC aggressiveness in a mA-dependent manner, providing novel biomarkers for BC diagnosis and therapy.

Further experiments demonstrated that LINC00520 could interact with RNA-binding protein LIN28B to inhibit autophagy and reduce DNA damage, thereby contributing to TMZ chemoresistance in GBM. These findings suggested that STAT3/LINC00520/LIN28B axis might be a promising target to improve TMZ chemoresistance of GBM.

The expression of LINC00520 is significantly related to the clinicopathological characteristics and prognosis of tumor patients and is also related to the sensitivity of HNSCC to radiotherapy. Here, this article summarizes the abnormal expression pattern of LINC00520 in cancer and its potential molecular regulation mechanism and points out that LINC00520 can be used as a potential biomarker for cancer diagnosis, prognosis, and treatment.

In conclusion, the inhibition of LINC00520 suppressed HCC cell proliferation, migration and invasion through mediating miR-4516/SOX5 axis. Therefore, our study provides a basis for the development of treatment strategies for HCC.

This study innovatively indicated that lncRNA LINC00520 facilitated cell proliferative and migratory abilities in LUAD through interacting with miR-3611 and targeting FOXP3, which may provide a potential novel insight for treatment of LUAD.

The positive regulation of autophagy may slow the transition from low-risk patients to high-risk patients in melanoma. Furthermore, compared with clinical information, the autophagy-related lncRNA risk model may better predict the prognosis of patients with melanoma and provide new treatment ideas.

Moreover, in NSCLC cells with si-LINC00520, up regulation of CCNE2 led to an increase of cell growth and invasion. Taken together, LINC00520 displayed its tumor-promotive roles through modulating the miR-577/CCNE2 axis, highlighting a potential therapeutic strategy for NSCLC patients.

Moreover, LINC00520 silencing suppressed the tumor growth of lung ADC in vivo. In summary, our data indicated that LINC00520 may act as a ceRNA to modulated FOXR2 level by sponging miR-1252-5p, which might bring a potential and effective biomarker to lung ADC treatment.

Moreover, these in vitro findings were reproduced in vivo in human HNSCC xenograft in nude mice. LINC00520/miR-195/HOXA10 is involved in the radiosensitivity mediation, providing potential therapeutic target for HNSCC treatment.

Rescue experiments revealed that inhibiting miR-577 or restoring HSP27 could abrogate the effects of LINC00520 silencing on malignant phenotypes of CRC. LINC00520 functioned as an oncogenic lncRNA in CRC, and it facilitated CRC progression by regulating the miR-577/HSP27 axis, suggesting that the LINC00520/miR-577/HSP27 axis is an effective target in anticancer management.

MiR-3175 inhibitor rescued the effect of si-LINC00520 on lung cancer progression. LncRNA LINC00520 could predict poor prognosis and promote progression of lung cancer by inhibiting miR-3175 expression.