miR-543 expression

Moreover, miR-543 affected HeLa cells by targeting HMGB2. In conclusion, circRNA THBS1 silencing inhibited the malignant biological behaviors of cervical cancer cells via the regulation of miR-543/HMGB2 axis.

Moreover, YAP1 overexpression could reverse the effects of SNHG6 downregulation on the malignant phenotypes of ovarian cancer cells. In summary, our study showed that SNHG6 promoted the malignant phenotypes of ovarian cancer cells via miR-543/YAP1 pathway.

TNRC6A knockdown reversed the effects of LINC01082 on the malignant character of NSCLC cells. In conclusion, LINC01082 exerts an antioncogenic role in NSCLC via interaction with miR-543 to regulate TNRC6A expression.

Our results suggest that microRNA-543, through the LINC00847/microRNA-543/STK31 axis, plays a role in the development of PC as a tumor suppressor. As a result, microRNA-543 may prove to be an effective diagnostic and therapeutic target for PC.

Meanwhile glioma cell apoptosis could be inhibited, and cell cycle arrest could be induced through this signaling pathway. circ-ASB3 could enhance glioma malignancy via miR-543/Twist1 axis, resulting in the discovery of new biomarkers and possible therapeutic targets for these patients.

Notably, upregulation of miR-543 led to increased cell supernatant glucose levels and suppressed cell growth, which was rescued by overexpression of IGF2. Exosomal miR-543 participates in the proteoglycan pathway to suppress cell proliferation by targeting IGF2 in OvCa.

miR-543 influences the biological behavior of TNBC cells by directly targeting ACTL6A gene. miR-543 could serve as a novel diagnostic and therapeutic target for TNBC.

The result after interfering with miR-543 is opposite, and luciferase reporter gene confirms that CDH2 is the target gene of miR-543. During the formation of intrauterine adhesions, the expression of CDH2, COL16A1, vimentin, and α-SMA may be inhibited by the high expression of miR-543, which may affect the degree of fibrosis and collagen content in the intrauterine adhesions, thereby inhibiting the occurrence and development of intrauterine adhesions.

Moreover, the effects of miR-543 upregulation and LINC01089 upregulation were mutually counteracted by each other. LINC01089 inhibited lung adenocarcinoma cell proliferation and promoted apoptosis via sponging miR-543.

The expression of miR-543 could also predict the survival of patients with PC, which suggested that miR-543 might play an important role in PC. The GO and KEGG pathway analysis also displayed that miR-543 was involved in several other pathways of pancreas.

MiR-543 participated in cell proliferation and metastasis by targeting PIAS3 in CRC.

This may be followed by increased expression of EMT causing cell migration and invasion. Consequently, miR-543 might be considered a therapeutic target for H. pylori-associated gastric cancer.