Taken together, the findings of this study reveal an oncogenic role for IL-21R in gastric tumorigenesis and verify that its activation is partly due to the dysregulation of the lncRNA MALAT1/miR-125a axis.
Notably, low DYNC1I1 expression in GBM cells coincided with more SK2 localized to the plasma membrane, where it has been recently implicated in oncogenesis.
The bidirectional gene pair PLAGL2/POFUT1 was subverted in CRC and acted synergistically to promote colorectal tumorigenesis by maintaining stemness of colorectal cancer stem cells through the Wnt and Notch pathways.
Pds5b (precocious dissociation of sisters 5B) is involved in both tumorigenesis and cancer progression; however, the functions and molecular mechanisms of Pds5b in pancreatic cancer (PC) are unknown.
Further investigations showed that SNAI3-AS1 could affect HCC tumorigenesis by binding up-frameshift protein 1 (UPF1), regulating Smad7 expression and activating TGF-β/Smad pathway.
CCK-8 assays, clonogenic survival assays, cell apoptosis analysis, wound healing assays and transwell invasion assays were used to examine the tumorigenesis function of miR-630 in vitro.
Our results indicate that LCPAT1, through RCC2 is involved in the CSE-induced DNA damage providing new insight into the lung carcinogenesis related to cigarette smoking.
Numerous studies have indicated that N-acetylglucosaminyltransferase V (MGAT5), is an important tumorigenesis and metastasis-associated enzyme in breast cancer (BC).
Dysregulation of miRNAs is critically implicated in tumorigenesis, and aberrant expression of miR-491-5p has been reported to play a key role in initiation and progression of various cancers.
Although nuclear type 2C protein phosphatase (PP2Cδ) has been demonstrated to be pro-oncogenic with an important role in tumorigenesis, the underlying mechanisms that link aberrant PP2Cδ levels with cancer development remain elusive.
Molecular mechanism demonstrated that hsa_circ_0001742 could directly bind to miR-634, which mediated the functions of hsa_circ_0001742 in TSCC tumorigenesis.
The smallest histone deacetylase (HDAC) and the only class IV HDAC member, HDAC11, is reported to regulate immune activation and tumorigenesis, yet its biochemical function is largely unknown.