Overexpression of LMP-1 Decreases Apoptosis in Human Nucleus Pulposus Cells via Suppressing the NF-κB Signaling Pathway.

Intervertebral disc degeneration (IDD) is a prevalent disease characterized by low back pain. Increasing extracellular matrix (ECM) synthesis and decreasing nucleus pulposus cell (NPC) apoptosis are promising strategies to recover degenerated NP. LIM mineralization protein- (LMP-) 1 has anti-inflammatory potential and is a promising gene target for the treatment of NP degeneration. In this study, we measured the expression of LMP-1 in the NP of patients. Then, we constructed LMP-1-overexpressing NPCs using lentiviral vectors and investigated the effects of LMP-1 on cell proliferation, apoptosis, and ECM synthesis in NPCs. The results showed that LMP-1 was highly expressed in the NP of patients. LMP-1 overexpression significantly increased proliferation and decreased apoptosis in NPCs. The expression of collagen II and sulfated glycosaminoglycan (sGAG) in NPCs was also upregulated after LMP-1 was overexpressed. Moreover, we demonstrated that LMP-1 decreased apoptosis of NPCs by inhibiting NF-κB signaling activation. These findings suggest that LMP-1 plays an essential role in mediating apoptosis in NPCs by regulating NF-κB signaling and can be used as a gene target for the treatment of IDD.

Long non-coding RNA FENDRR restrains the aggressiveness of CRC via regulating miR-18a-5p/ING4 axis.

There is increasing evidence has indicated that long non-coding RNAs (lncRNAs) are implicated in the tumorigenesis and development of colorectal cancer (CRC). Nevertheless, the clinical significances and functions of FENDRR in CRC remain unknown. In this study, we reveal that lncRNA FENDRR is downregulated in CRC and negatively correlated with advanced stage and poor clinical outcomes of patient with CRC. Overexpression of FENDRR represses the proliferation, migrate and invasive capacities of CRC cell in vitro, and upregulation of FENDRR inhibits the growth and distant metastatic capacity of CRC cell in vivo. Mechanistically, FENDRR interacts with miRNA-18a-5p (miR-18a-5p) and subsequently regulates the expression of inhibitor of growth 4 (ING4) in CRC cell. Interestingly, ING4 repression or miR-18a-5p rescues FENDRR induced proliferation and aggressive phenotypes inhibition of CRC cell. Altogether, our findings suggest that FENDRR exerts an inhibitory role in CRC by interacting with miR-18a-5p and future increases ING4 expression.