ZNF692 promotes colon adenocarcinoma cell growth and metastasis by activating the PI3K/AKT pathway

Abstract

Despite considerable recent advancements in colorectal cancer (CRC) therapy, the prognosis of patients with advanced disease remains poor. Further understanding of the molecular mechanisms and treatment strategies of this disease is required. Zinc finger protein 692 (ZNF692), also known as AREBP and Zfp692, was first reported to have an important role in gluconeogenesis. A recent study demonstrated that ZNF692 is overexpressed in lung adenocarcinoma (LUAD) tissues and that ZNF692 knockdown inhibited LUAD cell proliferation, migration, and invasion both in vitro and in vivo . However, the role of ZNF692 in colon adenocarcinoma (COAD) remains unclear. The present study revealed that ZNF692 was upregulated in COAD tissues and cells and that high ZNF692 expression was significantly correlated with lymph node metastasis, distant metastasis and tumor stage in COAD patients. Gain- and loss-of-function experiments were employed to identify the function of ZNF692 in COAD progression. In vitro and in vivo assays revealed that ZNF692 promoted COAD cell proliferation, migration and invasion. Furthermore, western blot analysis demonstrated that the effects of ZNF692 were mediated by upregulating cyclin D1, cyclin-dependent kinase 2 (CDK2) and matrix metalloproteinase-9 (MMP-9) and by downregulating p27 Kip1 through the phosphoinositide 3-kinase/AKT signaling pathway. Collectively, these data indicated that ZNF692 may serve as a novel oncogene and a potential treatment target in COAD patients.

The role of circular RNA circ_0008285 in gestational diabetes mellitus by regulating the biological functions of trophoblasts

“…It has been confirmed that the PI3K/Akt pathway activation plays an important role in promoting placental development, fetal growth, and GDM in humans and rodents [ 34 , 35 ]. Moreover, the PI3K/Akt signaling pathway is important for cell proliferation, migration, invasion, and gluconeogenesis [ 36 ]. Past studies have demonstrated that the inhibition of the PI3K/Akt signaling pathway can reduce oxidative stress, affect the function of trophoblast cells, and reduce the blood glucose level in a GDM rat model [ 37 ].…”

CYP2E1 changes the biological function of gastric cancer cells via the PI3K/Akt/mTOR signaling pathway

“…Pi3K/akt/mTor is a crucial signaling pathway involved in the carcinogenicity and tumorigenesis of different cancer types, and is closely related to cell biological functions, such as energy metabolism, proliferation, apoptosis and cell invasion (16)(17)(18)(19). Previous studies have revealed that certain mrnas are co-expressed with cYP2e1 and participate in the Pi3K/akt/mTor signaling pathway (20,21).…”

Diagnostic significance and carcinogenic mechanism of pan‐cancer gene POU5F1 in liver hepatocellular carcinoma

“…CBX3 has been confirmed to promote cell cycle transition by inducing CDK1 and PCNA 79 . The elevated POU5F1 in LIHC may influence the expression of CBX3 and then activate the NF‐Kβ and PI3K/Akt pathways through BARD1 and ZNF692 80,81 . The promotion effect of CCND2 on cell proliferation is regulated by NFYC and may also be affected by POU5F1 82 .…”

“…79 The elevated POU5F1 in LIHC may influence the expression of CBX3 and then activate the NF-Kβ and PI3K/Akt pathways through BARD1 and ZNF692. 80,81 The promotion effect of CCND2 on cell proliferation is regulated by NFYC and may also be affected by POU5F1. 82 The interaction between NFYC and KAT2A indicates that POU5F1 participates in tumor development through KAT2A-mediated histone H3 succinylation.…”