hmiR-34c-3p upregulation inhibits the proliferation of colon cancer cells by targeting EIF3D

Abstract

Our study desired to investigate how miR-34c-3p regulates colon cancer cell proliferation and what is the relationship between miR-34c-3p and EIF3D. HCEpiC (normal human colonic epithelial cells), SW620, HT-29, SW480, and HCT-116 (human colon cancer cells lines) were used in our study. SW620 cells were chosen and divided into blank, miR-34c-3p mimics, miR-34c-3p NC, miR-34c-3p inhibitors, Lv-EIF3D, Lv-NC, and miR-34c-3p mimics+Lv-EIF3D groups. qRT-PCR was used for the detection of miR-34c-3p and EIF3D mRNA expressions. Dual-luciferase reporter assay was performed to investigate the effect of miR-34c-3p on EIF3D. Western blot was performed to detect EIF3D, cyclin D1, and c-Myc expressions. Clone formation and MTT assay were used to measure cell proliferation ability. colon cancer cells had lower miR-34c-3p expression, but higher EIF3D expression compared with HCEpiC. EIF3D mRNA expression was regulated negatively by miR-34c-3p. In the miR-34c-3p mimics group, colon cancer cell proliferation was significantly decreased, whereas c-Myc and cyclin D1 expressions were downregulated. Colon cancer cell proliferation in miR-34c-3p inhibitors and Lv-EIF3D groups was enhanced, and c-Myc and cyclin D1 expressions were decreased. The results suggested that by targeting EIF3D, miR-34c-3p inhibited colon cancer cell proliferation.

MiR-34c-3p targets Notch2 to inhibit cell invasion and epithelial-mesenchymal transition in nasopharyngeal carcinoma

“…Human miR-34c-3p gene locates in 11q23.1 region in chromosomes and is highly conservative. Studies in recent years reveal that expression of miR-34c-3p is down-regulated in lung cancer, colorectal cancer, liver cancer, breast cancer, prostate cancer, ovarian cancer, and is related to tumor invasion and metastasis (Russo et al, 2018;Du et al, 2018;Xiao et al, 2017;Wu et al, 2017). This study indicated that miR-34c was downregulated in NPC and up-regulated in PT, while Notch2 was up-regulated in NPC and down-regulated in PT, which suggested that miR-34c-3p might be related to the carcinogenesis of NPC.…”

EIF3D promotes resistance to 5‐fluorouracil in colorectal cancer through upregulating RUVBL1

“…Previous studies on CRC have confirmed that EIF3D plays a carcinogenic role, with a high expression in CRC cells. 19 , 32 To verify the expression pattern of EIF3D in CRC, CRC cells and tissues were subjected to qRT‐PCR, after which the expression level of EIF3D was observed to be higher in CRC tissues and CRC cells (HCT116, HCT15, SW480, SW620, and LOVO) than in the para‐cancerous tissues and CCD‐18Co cells (Figure 1A,B , p < 0.001). Of note, EIF3D has been proposed as the culprit to induce multidrug resistance during treatment of several cancers.…”

“… 11 , 12 EIF3, the first identified EIFs, has 13 subunits, one of which is eukaryotic translation initiation factor 3D (EIF3D). 13 Abnormally highly expressed EIF3D has been reported to be relevant to the occurrence and malignant progression of gallbladder cancer, 14 bladder cancer, 15 breast cancer, 16 prostate cancer, 17 non‐small‐cell lung cancer 18 and CRC, 19 and found to result in sunitinib resistance on renal cell carcinoma (RCC). 20 Currently, in CRC, an oncogenic role of EIF3D has been identified, while how EIF3D regulates apoptosis during chemotherapy resistance has yet to be investigated.…”

Overexpression of Eukaryotic translation initiation factor 3D induces stem cell-like properties and metastasis in cervix cancer by activating FAK through inhibiting degradation of GRP78

“…Depletion of ELF3D could inhibit the proliferation and migration of breast cancer cells by inhibiting the Wnt/β-catenin pathway [ 11 ]. In addition, ELF3D was significantly associated with the poor prognosis of patients with multiple cancers [ 12 , 13 ]. Notably, TCGA database analysis showed that ELF3D was highly expressed in cervix cancer.…”