Ask about this productRelated genes to: TMEM93 antibody
- Gene:
- EMC6 NIH gene
- Name:
- ER membrane protein complex subunit 6
- Previous symbol:
- TMEM93
- Synonyms:
- MGC2963, RAB5IFL
- Chromosome:
- 17p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-12-13
- Date modifiied:
- 2018-02-16
Related products to: TMEM93 antibody
Related articles to: TMEM93 antibody
- The endoplasmic reticulum (ER) membrane protein complex (EMC) is an ER multiprotein complex that affects a wide range of pathophysiological processes. Recently, the function of EMC6, a subunit of EMC, has been attracting attention for its role in cancers. However, research on EMC6 in the context of hepatocellular carcinoma (HCC) remains unknown. Here, we first observed the decreased EMC6 expression in human HCC tissues, and diminished expression level of EMC6 was associated with poor prognosis of HCC patients. In parallel, the knockdown of EMC6 promoted tumor progression both in HCC cell lines and in tumor-cell bearing nude mice. To delineate the in vivo roles of EMC6, we generated a hepatocyte-specific knockout of Emc6 (Emc6;Alb-Cre, named Emc6 LKO) using a floxed Emc6 line. Emc6 LKO mice exhibited progressive liver dysfunction, fibrosis and spontaneous carcinogenesis phenotypes. Significant lipid metabolic disorder in the Emc6 LKO liver was revealed by combined metabolomic and proteomic analysis. Moreover, drastic elevation of 17β-Hydroxysteroid dehydrogenase type 13 (HSD17B13), a lipid droplet-associated enzyme, was identified to be involved in the process of EMC6-induced lipid metabolic disorder and HCC progression. Inhibition of HSD17B13 by a Pharmacological inhibitor BI-3231 effectively mitigated EMC6-driven HCC progression in vitro and in vivo. Taken together, these results unveiled a novel regulatory mechanism of EMC in HCC progression through lipid metabolism and may provide a new biomarker and therapeutic target for HCC. - Source: PubMed
Publication date: 2025/12/03
Zhang YunXiong ChanyuJiang ZhilinWang XiaoWang ZihaoChen JunyaoLi QiongLuo YangyangYang XudanChu ChenZhu ShikaiZhu XianjunZhou Yu - Endometrial cancer (EC) is a common gynecological cancer worldwide, often associated with a poor prognosis after recurrence or metastasis. Ovatodiolide (OVA) is a macrocyclic diterpenoid derived from Anisomeles indica that shows anticancer effects in various malignancies. This study aimed to evaluate the cytotoxic effects of OVA on EC cell proliferation and cancer stem cell (CSC) activity and explore its underlying molecular mechanisms. OVA treatment dose-dependently reduced the viability and colony formation of three EC cell lines (AN3CA, HEC-1A, and EMC6). It induced G2/M phase cell cycle arrest, associated with decreased cell division cycle 25C (CDC25C) expression and reduced activation of cyclin-dependent kinases 1 (CDK1) and 2 (CDK2). OVA also increased reactive oxygen species (ROS) production and DNA damage, activating the DNA damage-sensitive cell cycle checkpoint kinases 1 (CHK1) and 2 (CHK2) and upregulating the DNA damage marker γ-H2A.X variant histone (H2AX). It also suppressed the activation of mechanistic target of rapamycin kinase (mTOR) and nuclear factor kappa B (NF-κB) and downregulated glutathione peroxidase 1 (GPX1), an antioxidant enzyme counteracting oxidative stress. Moreover, OVA reduced the self-renewal capacity of CSCs, reducing the expression of key stemness proteins Nanog homeobox (NANOG) and octamer-binding transcription factor 4 (OCT4). The ROS inhibitor N-acetylcysteine attenuated the anti-proliferative and anti-CSC effects of OVA. Our findings suggest that OVA acts via ROS generation, leading to oxidative stress and DNA damage, culminating in cell cycle arrest and the suppression of CSC activity in EC. Therefore, OVA is a promising therapeutic agent for EC, either as a standalone treatment or an adjunct to existing therapies. - Source: PubMed
Publication date: 2024/09/12
Chen Chun-YuYe Yu-ZhenHuang Yu-HaoTzeng Yew-MinGurbanov RanalWang Wen-LingChang Wen-Wei - Ubiquitin A-52 residue ribosomal protein fusion product 1 (UBA52) has a role in the occurrence and development of tumours. However, the mechanism by which UBA52 regulates hepatocellular carcinoma (HCC) tumorigenesis and progression remains poorly understood. By using the Cell Counting Kit (CCK-8), colony formation, wound healing and Transwell assays, we assessed the effects of UBA52 knockdown and overexpression on the proliferation and migration of HCC cells in vitro. By establishing subcutaneous and metastatic tumour models in nude mice, we evaluated the effects of UBA52 on HCC cell proliferation and migration in vivo. Through bioinformatic analysis of data from the Gene Expression Profiling Interactive Analysis (GEPIA) and The Cancer Genome Atlas (TCGA) databases, we discovered that UBA52 is associated with autophagy. In addition, we discovered that HCC tissues with high UBA52 expression had a poor prognosis in patients. Moreover, knockdown of UBA52 reduced HCC cell growth and metastasis both in vitro and in vivo. Mechanistically, knockdown of UBA52 induced autophagy through EMC6 in HCC cells. These findings suggest that UBA52 promoted the proliferation and migration of HCC cells through autophagy regulation via EMC6 and imply that UBA52 may be a viable novel treatment target for HCC patients. - Source: PubMed
Tong LiZheng XiaofeiWang TianqiGu WangShen TingtingYuan WenkangWang SiyuXing SonglinLiu XiaoyingZhang ChongZhang Chao - Endoplasmic reticulum membrane protein complex subunit 6 (EMC6) plays an important function in both physiological and pathological states of cells. Nevertheless, there are few studies focused on the role of EMC6 in tumors. At first, we performed a series of bioinformatics analyses on 33 kinds of cancers, including differential expression analysis, tumor mutational burden analysis, prognostic analysis, and clinicopathological staging analysis. Then, we corroborated the important role of EMC6 in lung cancer by cytological and experiments. We found that the reduction of EMC6 expression did effectively inhibit the proliferation, invasion, and metastasis of A549. Finally, EMC6 is indeed involved in the regulation of ferroptosis, cuproptosis, and immune response in LUAD. In a word, our study not only comprehensively analyzed the functional mechanisms of EMC6 in all cancers but also validated the regulatory role of EMC6 in lung cancer for the first time. - Source: PubMed
Publication date: 2023/12/08
Zhou XinXiao BowenJiang ManmanRui Jun - The endoplasmic reticulum (ER) membrane protein complex (EMC) is responsible for monitoring the biogenesis and synthetic quality of membrane proteins with tail-anchored or multiple transmembrane domains. The EMC subunit EMC6 is one of the core members of EMC and forms an enclosed hydrophilic vestibule in cooperation with EMC3. Despite studies demonstrating that deletion of EMC3 led to rhodopsin mislocalization in rod photoreceptors of mice, the precise mechanism leading to the failure of rhodopsin trafficking remains unclear. Here, we generated the first rod photoreceptor-specific knockout of (RKO) and cone photoreceptor-specific knockout of (CKO) mouse models. Deficiency of in rod photoreceptors led to progressive shortening of outer segments (OS), impaired visual function, mislocalization and reduced expression of rhodopsin, and increased gliosis in rod photoreceptors. In addition, CKO mice displayed the progressive death of cone photoreceptors and abnormal localization of cone opsin protein. Subsequently, proteomics analysis of the RKO mouse retina illustrated that several cilium-related proteins, particularly anoctamin-2 (ANO2) and transmembrane protein 67 (TMEM67), were significantly down-regulated prior to OS degeneration. Detrimental rod photoreceptor cilia and mislocalized membrane disc proteins were evident in RKO mice. Our data revealed that in addition to monitoring the synthesis of rhodopsin-dominated membrane disc proteins, EMC6 also impacted rod photoreceptors' ciliogenesis by regulating the synthesis of membrane proteins associated with cilia, contributing to the mislocalization of membrane disc proteins. - Source: PubMed
Publication date: 2023/05/23
Sun KuanxiangLiu LuJiang XiaoyanWang HetingWang LinYang YemingLiu WenjingZhang LinZhao XiaohuiZhu Xianjun