Tripartite motif‑containing 14 regulates cell proliferation and apoptosis in cervical cancer via the Akt signaling pathway

Abstract

Tripartite motif-containing (TriM) 14 is a protein of the TriM family. Studies have indicated that TriM14 may be used as an oncogene in tumor cells, such as osteosarcoma, non-small cell lung cancer and breast cancer through different pathways. However, the functions of TriM14 in cervical cancer cells remain unclear. Therefore, this study aimed to investigate the functions of TriM14 in cervical cancer cells and its underlying mechanism. caski cells stably expressing TriM14 and SiHa, and Hela cells stably expressing TriM14 short hairpin rna were constructed by lentivirus-mediated overexpression or knockdown systems. The effects of TriM14 on proliferation and apoptosis of cervical cancer cells were detected by cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. in addition, reverse transcription-quantitative (rT-q) Pcr and western blotting were used to investigate the expression levels of TriM14 and of signaling pathway marker protein including P21, caspase-3, cleaved caspase-3, akt and phosphorylated akt. The results of rT-qPcr and western blotting revealed that TriM14 was highly expressed in human cervical cancer tissues and cell lines compared with adjacent normal tissues and normal cervical epithelial cells. TriM14 also regulated cell proliferation and apoptosis of human SiHa, Hela and caski cervical cancer cell lines through the akt signaling pathway. additionally, TriM14 protein levels were related to the clinical and pathological features of cervical cancer. CCK-8 assay and flow cytometry demonstrated that TRIM14 expression could promote cervical cancer cell proliferation and autophagy suppression. Taken together, TriM14-induced cell proliferation and apoptosis inhibition may by evoked by the activation of the akt pathway. This study demonstrated the role of TriM14 in cervical cancer, and reveals its mechanism of action as a potential therapeutic target for cervical cancer.

TRIM14 Overexpression Induces Chemoresistance and Malignant Behaviors of Hepatocellular Carcinoma Cells by Activating the STAT3/HIF-1α Pathway

“…TRIM protein families pertain to the pathogenesis of multiple human cancers, taking part in the modulation of many cellular functions. For instance, TRIM14 expression is elevated in diverse cancers, such as gastric cancer and cervical cancer [ 18 , 19 ]. Overexpressed TRIM14 can bolster breast cancer cell proliferation, adding to the malignancy of colorectal cancer [ 20 , 21 ].…”

Multipronged regulation of autophagy and apoptosis: emerging role of TRIM proteins

“…In addition, it also controls the levels of the MDM2 protooncogene (MDM2) and AKT serine/threonine kinase 1 (AKT1), thereby increasing the levels of TP53, BAX, and cyclin-dependent kinase inhibitor 1A (CDKN1A), leading to increased apoptosis under ionizing radiation [ 167 , 168 ]. Diao et al reported that TRIM14 is highly expressed in human cervical cancer cells and regulates cell proliferation and death through the AKT1 pathway [ 169 ]. In contrast, TRIM14 is inhibited to protect against cerebral ischemia injury, which is regulated by NFKB/NLRP pathway-mediated apoptosis [ 170 ].…”

Advances in the antitumor mechanisms of tripartite motif-containing protein 3

“…This inhibition is accomplished through the regulation of transcription factors and mediation of signaling molecules crucial for the EMT process, which is essential for cell migration and invasion. Notably, TRIM3 downregulates the expression of EMT transcription factors, such as Snail, Slug, and TWIST, thus curbing the EMT process in cervical cancer cells and weakening their migration and invasion potentials (Diao et al 2020 ). Furthermore, TRIM3 overexpression exhibits tumor-inhibiting effects in cervical cancer.…”

“…Furthermore, TRIM3 overexpression exhibits tumor-inhibiting effects in cervical cancer. Research reveals that TRIM3 reduces the population of cervical cancer tumor stem cells and actively participates in regulating their apoptosis and differentiation by engaging various signaling pathways (Diao et al 2020 ). Moreover, TRIM3 overexpression effectively suppresses angiogenesis, resulting in decreased tumor blood supply and growth.…”