MIR876 (MicroRNA 876)

LINC00519 upregulation may serve as a potential indicator of CCA aggravation. LINC00519 promoted CCA development by targeting miR-876-3p to affect cancer cell activities. GATA1, a potential target of miR-876-3p, suggests the potential underlying molecular pathway. Targeting LINC00519 could be an efficient way to manage CCA.

miR-876-3p could reverse the functions of HOXC-AS1 for HCC cells by targeting NR3C1. Upregulation of HOXC-AS1 promotes HCC progression through the miR-876-3p/NR3C1 axis.

Meanwhile, MINCR silencing or miR-876-5p overexpression synergized with GEM to depress BC growth in vivo. MINCR silencing impedes GEM resistance in BC through the miR-876-5p/ZEB1/PHGDH axis.

Clinically, high hsa_circ_103089 expression correlated with poor prognosis in NSCLC patients. These findings establish hsa_circ_103089 as a critical regulator of NSCLC progression and chemoresistance via the miR-876-5p/EGFR axis, highlighting its potential as a prognostic biomarker and therapeutic target.

Our results identified promising biomarkers that play a role in specific groups of prostate cancer patients. Detecting specific biomarkers may be an effective strategy for different groups of PC patients.

Additionally, exposure to the tobacco-specific carcinogen NNK was found to induce miR-876 expression and STAT3 activation, implicating environmental factors in miR-876 regulation and promote cancer recurrent. These findings identify the miR-876-5p-SOCS4-STAT3 axis as a critical pathway in OSCC progression, highlighting miR-876-5p as a potential biomarker and therapeutic target to improve treatment outcomes in OSCC patients.

On the mechanism, ABHD11-AS1 elevated CALM2 and promoted the malignant development of TC cells by acting as a miR-876-5p sponge. ABHD11-AS1 mediated the miR-876-5p/CALM2 axis to drive the metastasis of thyroid cancer.

Both in vitro and in vivo studies revealed that overexpression of TCL6 suppressed tumor growth and improved the response to PD-1 immunotherapy in tumor-bearing mice. This research highlights the pivotal role of lncRNA TCL6 in breast cancer development via a ceRNA network involving miR-876-5p and MYL2, suggesting a novel molecular target for breast cancer therapy.

These studies identify miR-876 as a distinct tumor suppressor on 9p21 that is inactivated in melanoma and suggest miR-876 loss as an additional mechanism to activate ERK and the mitogen activated protein kinase (MAPK) pathway in melanoma. In addition, they suggest the therapeutic potential of combining miR-876 overexpression with BRAF inhibition as a rational therapeutic strategy for melanoma.

In addition, circTLK1 interacted with miR-876-3p, and SRSF7 was concluded to be the target gene of miR-876-3p. In this study, we researched the inhibitory effect of circTLK1knockdown on NSCLC progression and immune escape, and further elucidated the potential regulatory mechanism of circTLK1/miR876-3p/SRSF7 axis.

CDKN3 overexpression can reverse the impacts of circ-NAB1 depletion on EC cell behaviors. Collectively, we proved that ALKBH5-mediated m6A modification of circ-NAB1 promoted EMT process and cell cycle in EC via targeting the miR-876-3p/CDKN3 axis.

Circ-POSTN knockdown inhibited proliferation and invasion, but increased apoptosis and enhanced radiosensitivity in EC cells via modulating miR-876-5p/FYN axis, which might be a potential diagnostic and therapeutic target for EC.