Overexpression of MALAT1 contributes to cervical cancer progression by acting as a sponge of miR-429

Cervical cancer remains a malignant type of tumor and is the fourth leading cause of cancer-related death among females. MALAT1 has been identified as a tumor oncogene in various cancers. Our present study aimed to explore the biological role of MALAT1 in cervical cancer. We observed that MALAT1 was significantly upregulated in human cervical cancer cell lines compared with the ectocervical epithelial cells. MALAT1 was repressed by transfection with LV-shMALAT1, whereas increased by LV-MALAT1 in HeLa and Caski cells. Silencing of MALAT1 obviously reduced cervical cell viability, induced cell apoptosis, and repressed cell invasion capacity. Conversely, overexpression of MALAT1 exhibited an opposite phenomenon. Furthermore, miR-429 was predicted as a direct target of MALAT1, and it was dramatically decreased in cervical cancer cells. It has been shown that miR-429 plays a crucial role in cervical cancer progression. In our current study, the targeting correlation between MALAT1 and miR-429 was confirmed by luciferase reporter assays and RIP experiments. Finally, in vivo animal models were established, and we indicated that MALAT1 inhibited cervical cancer progression via targeting miR-429. These findings revealed that MALAT1 can sponge miR-429 and regulate cervical cancer pathogenesis in vivo and in vitro. In conclusion, we indicated that the MALAT1/miR-429 axis was involved in cervical cancer development.     

Long noncoding RNA ZEB1-AS1 attenuates ferroptosis of gastric cancer cells through modulating miR-429/BGN axis

Gastric cancer (GC) is the fifth utmost common malignant cancer type globally, in which ferroptosis acts a critical function in the progress of GC. Long noncoding RNA ZEB1-AS1 has been recognized in numerous cancers, but the role of ZEB1-AS1 in ferroptosis remains obscure. Hence, we investigated the efficacy of ZEB1-AS1 on ferroptosis of GC cells. The cell growth and viability were analyzed via cell counting kit assay and xenograft tumor model in vivo and in vitro, respectively. The RNA and protein expression were measured by qRT-PCR and western blot analysis assay, respectively. The levels of Fe²⁺, malondialdehyde (MDA), and lipid reactive oxygen species (ROS) were tested to determine ferroptosis. The erastin and RSL3 were used to induce ferroptosis. The mechanism was analyzed via luciferase reporter gene and RIP assays. The treatment of ferroptosis inducer Erastin and RSL3 suppressed the viability of GC cells and the ZEB1-AS1 overexpression rescued the phenotype in the cells. The levels of Fe²⁺, MDA, and ROS were enhanced through the depletion of ZEB1-AS1 in Erastin/RSL3 treated GC cells. ZEB1-AS1 directly sponged miR-429 in GC cells and miR-429 targeted BGN in GC cells, and the inhibition of miR-429 rescued ZEB1-AS1 depletion-inhibited BGN expression. We validated that miR-429 induced and BGN-repressed ferroptosis in cancer cells. The BGN overexpression and miR-429 suppression could reverse the efficacy of ZEB1-AS1 on proliferation and ferroptosis in cancer cells. The expression of ZEB1-AS1 and BGN was enhanced and miR-429 expression was decreased in clinical GC tissues. ZEB1-AS1 attenuated ferroptosis of cancer cells by modulating miR-429/BGN axis.     

SARS-CoV-2 spike L452R variant evades cellular immunity and increases infectivity

1. Download : Download high-res image (197KB)
2. Download : Download full-size image

     

MiR‐429 suppresses glioblastoma multiforme by targeting SOX2

Accumulating evidence has shown that miR‐429 plays an important role in the development and progression of tumour. However, the role of miR‐429 in glioblastoma multiforme (GBM) remains largely unknown. The present study is designed to investigate the function of miR‐429 in GBM and to explore the molecular mechanism underlying its function. The expression level of miR‐429 was detected in GBM tissues and cell lines by quantitative real‐time polymerase chain reaction. The effect of overexpression of miR‐429 on in vitro cell proliferation, apoptosis and invasion was examined. Western blot analysis was used to detect the influence of miR‐429 on the expression of target gene, and Pearson analysis was used to calculate the correlation between the expression of targets gene and the miR‐429 in GBM tissues. Our study shows that miR‐429 is downregulated in GBM tissues compared with noncancerous tissues (P < .01). In addition, the expression of miR‐429 in GBM cell lines is also significantly lower (P < .01). Enforced expression of miR‐429 inhibits GBM cells proliferation, induces apoptosis and suppresses invasion and leads to the downregulation of the SOX2 protein. Moreover, the expression level of miR‐429 in GBM tissues shows inverse relationship with the expression level of SOX2 protein. Our findings suggest that miR‐429 represents a potential tumour‐suppressive miRNA and plays an important role in GBM progression by directly targeting SOX2.