SOGA1

更新于：2025-05-07

基本信息

别名

80-kDa SOGA fragment、C-terminal 80 kDa form、C20orf117

+ [11]

简介

Microtubule-associated factor that enables integration of the centrosomal and Golgi-associated microtubules on the Golgi membrane, supporting directional migration. Preferentially acts on the perinuclear microtubules accumulated around the Golgi. Associates with the Golgi membrane through the N-terminal coiled-coil region and directly binds microtubules through the C-terminal domain (By similarity). Required for faithful chromosome segregation during mitosis (PubMed:33587225). Regulates autophagy by playing a role in the reduction of glucose production in an adiponectin- and insulin-dependent manner (By similarity).

关联

100 项与 SOGA1 相关的临床结果

登录后查看更多信息

100 项与 SOGA1 相关的转化医学

登录后查看更多信息

0 项与 SOGA1 相关的专利（医药）

登录后查看更多信息

项与 SOGA1 相关的文献（医药）

2024-05-01·Cell Proliferation

METTL16‐mediated N6‐methyladenosine modification of Soga1 enables proper chromosome segregation and chromosomal stability in colorectal cancer

Article

作者: Li, Jimin ; Wang, Zeyu ; Yang, Fang ; Wang, Hao ; Wang, Chen ; Zhang, Shuang ; Zheng, Siqing ; He, Bing ; Wang, Jia-Bei

AbstractN6‐methyladenosine (m6A) is the most prevalent internal modification in mammalian messenger RNAs and is associated with numerous biological processes. However, its role in chromosomal instability remains to be established. Here, we report that an RNA m6A methyltransferase, METTL16, plays an indispensable role in the progression of chromosome segregation and is required to preserve chromosome stability in colorectal cancer (CRC) cells. Depletion or inhibition of the methyltransferase activity of METTL16 results in abnormal kinetochore‐microtubule attachment during mitosis, leading to delayed mitosis, lagging chromosomes, chromosome mis‐segregation and chromosomal instability. Mechanistically, METTL16 exerts its oncogenic effects by enhancing the expression of suppressor of glucose by autophagy 1 (Soga1) in an m6A‐dependent manner. CDK1 phosphorylates Soga1, thereby triggering its direct interaction with the polo box domain of PLK1. This interaction facilitates PLK1 activation and promotes mitotic progression. Therefore, targeting the METTL16‐Soga1 pathway may provide a potential treatment strategy against CRC because of its essential role in maintaining chromosomal stability.

2024-01-01·Bioengineering & Translational Medicine

An engineered niche delineates metastatic potential of breast cancer

Article

作者: DeVaull, Christian Y. ; Shea, Lonnie D. ; Bealer, Elizabeth J. ; Orbach, Sophia M. ; Jeruss, Jacqueline S. ; Ross, Brian C.

AbstractMetastatic breast cancer is often not diagnosed until secondary tumors have become macroscopically visible and millions of tumor cells have invaded distant tissues. Yet, metastasis is initiated by a cascade of events leading to formation of the pre‐metastatic niche, which can precede tumor formation by a matter of years. We aimed to distinguish the potential for metastatic disease from nonmetastatic disease at early times in triple‐negative breast cancer using sister cell lines 4T1 (metastatic), 4T07 (invasive, nonmetastatic), and 67NR (nonmetastatic). We used a porous, polycaprolactone scaffold, that serves as an engineered metastatic niche, to identify metastatic disease through the characteristics of the microenvironment. Analysis of the immune cell composition at the scaffold was able to distinguish noninvasive 67NR tumor‐bearing mice from 4T07 and 4T1 tumor‐bearing mice but could not delineate metastatic potential between the two invasive cell lines. Gene expression in the scaffolds correlated with the up‐regulation of cancer hallmarks (e.g., angiogenesis, hypoxia) in the 4T1 mice relative to 4T07 mice. We developed a 9‐gene signature (Dhx9, Dusp12, Fth1, Ifitm1, Ndufs1, Pja2, Slc1a3, Soga1, Spon2) that successfully distinguished 4T1 disease from 67NR or 4T07 disease throughout metastatic progression. Furthermore, this signature proved highly effective at distinguishing diseased lungs in publicly available datasets of mouse models of metastatic breast cancer and in human models of lung cancer. The early and accurate detection of metastatic disease that could lead to early treatment has the potential to improve patient outcomes and quality of life.

2021-03-01·Molecular Biology Reports4区 · 生物学

Biomarker potentials of miRNA-associated circRNAs in breast cancer (MCF-7) cells: an in vitro and in silico study

4区 · 生物学

Article

作者: Aliyazicioglu, Yuksel ; Misir, Sema ; Hepokur, Ceylan ; Enguita, Francisco J

Breast cancer is a heterogeneous disease, which is the most common malignancy in women. The incidence and mortality rates of breast cancer indicate that it is the leading cause of cancer-related with deaths. circRNAs operate as part of competing endogenous RNAs (ceRNAs) mechanisms, which play critical roles in the different biological processes of breast cancer such as proliferation, migration, and apoptosis. The goal of the present study is to identify the potential predictive biomarker for breast cancer diagnosis in the circRNA network by in vitro and in silico analyzes. 40 miRNAs were obtained from the miRWalk database and their combinatorial target genes (potential ceRNAs) were identified with ComiR. We stated that the cancer-specific circRNA genes in MCF-7 cells using the cancer-specific circRNA (CSDC) database, and obtained the ones showing potential ceRNA activity in our previous analysis among them. Identified genes with remarkable expression differences between BCa and normal breast tissue were determined by the GEPIA database. Moreover, the Spearman correlation test in the GEPIA database was used for the statistical analysis of the relationship between DCAF7 and SOGA1, SOGA1 and AVL 9, DCAF7 and AVL 9 gene pairs. And also, DCAF7, SOGA1, and AVL9 gene expression levels were detected in MCF-7 and MCF-10A cells by RT-qPCR method. DCAF7, SOGA1, and AVL9 gene were significantly more expressed to BCa tissue and MCF-7 cells than normal breast tissue and MCF-10 A cells. And also, DCAF7 and SOGA1, SOGA1 and AVL9, DCAF7 and AVL9 genes pairs were found to be significantly correlated with BCa. These genes may be considered as potential predictive biomarkers to discriminate BCa patients from healthy persons. Our preliminary results can supply a new perspective for in vitro and vivo studies in the future.

项与 SOGA1 相关的新闻（医药）

2023-07-17

·生物谷

中国科技大学研究者们揭示了METTL16促进糖酵解代谢重编程与结直肠癌进展

结直肠癌(CRC)是人类第四大常见恶性肿瘤，也是全球第三大癌症相关死亡原因。结直肠癌是一种多因素疾病，涉及遗传、遗传、环境和生活方式等危险因素。结直肠癌(CRC)是人类第四大常见恶性肿瘤，也是全球第三大癌症相关死亡原因。结直肠癌是一种多因素疾病，涉及遗传、遗传、环境和生活方式等危险因素。大多数结直肠癌是散发性的，WNT、EGFR、P53、转化生长因子-β信号通路的突变顺序累积，APC、KRAS、BRAF和DNA错配修复基因被发现导致结直肠癌的发生和发展。除了这些遗传事件，详尽的转录分析显示，根据独特的克隆性、间质和免疫依赖性，结直肠癌的分子分类具有共识，有四种共识的分子亚型。这些共有的分子亚型概括了在结直肠癌中观察到的异质性，并预测了靶向治疗的反应。所有这些都极大地促进了对结直肠癌的诊断和治疗。然而，尤其是在晚期，由于缺乏早期诊断和有效的干预措施，结直肠癌变得难以治疗，导致转移，预后较差。这些糟糕的治疗结果突出表明，需要更好地了解导致结直肠癌启动、进展和扩散的机制。图片来源: https://doi.org/10.1186/s13046-023-02732-y 近日，来自中国科学技术大学的研究者们在J Exp Clin Cancer Res杂志上发表了题为“METTL16 promotes glycolytic metabolism reprogramming and colorectal cancer progression”的文章，该研究结果表明，METTL16/SOGA1/PDK4轴可能是治疗结直肠癌的有效靶点。糖酵解是癌症的关键标志，并维持恶性肿瘤的发生和发展。N6-甲基腺苷(M6A)修饰在糖酵解中的作用在很大程度上是未知的。本研究探讨了M6A甲基转移酶METTL16在糖酵解代谢中的生物学作用，揭示了结直肠癌发生发展的新机制。研究者们用生物信息学和免疫组织化学(IHC)方法评价METTL16的表达和预后价值。分析METTL16在体内和体外对结直肠癌进展的生物学作用。糖酵解代谢实验验证METTL16和自噬葡萄糖抑制因子(SOGA1)的生物学功能。通过蛋白质/RNA稳定性、RNA免疫沉淀(RIP)、共免疫沉淀(Co-IP)和RNA下拉实验，探讨了其可能的分子机制。 SOGA1是METTL16的直接下游靶点，参与METTL16介导的糖酵解和结直肠癌进展。METTL16通过结合“阅读器”蛋白胰岛素样生长因子2mRNA结合蛋白1(IGF2BP1)显著增强SOGA1的表达和mRNA的稳定性。随后，SOGA1促进AMPK复合体的泛素化，抑制AMPK的表达和磷酸化，从而上调控制糖代谢的关键蛋白丙酮酸脱氢酶激酶4(PDK4)。此外， YY1可通过直接与其启动子结合而转录抑制结直肠癌细胞中METTL16的表达。临床资料表明，METTL16的表达与SOGA1、PDK4呈正相关，与结直肠癌患者的预后不良有关。 METTL16促进的SOGA1 M6A修饰在CRC进展中的机制总结图片来源: https://doi.org/10.1186/s13046-023-02732-y 本研究结果表明，METTL16在结直肠癌进展中具有促进肿瘤的作用。METTL16在结直肠癌组织中表达上调，与结直肠癌患者的预后不良有关。从机制上讲，METTL16/SOGA1/PDK4信号轴通过诱导糖酵解促进结直肠癌进展。这一发现为探索新的结直肠癌诊断生物标记物和治疗靶点提供了新的见解。（生物谷 Bioon.com）参考文献 Wei Wei et al. METTL16 promotes glycolytic metabolism reprogramming and colorectal cancer progression. J Exp Clin Cancer Res. 2023 Jun 20;42(1):151. doi: 10.1186/s13046-023-02732-y.

临床研究

2023-07-10

·生物谷

结直肠癌(CRC)是人类第四大常见恶性肿瘤，也是全球第三大致死癌症。结直肠癌是一种多因素疾病，涉及遗传、遗传、环境和生活方式等危险因素。结直肠癌(CRC)是人类第四大常见恶性肿瘤，也是全球第三大致死癌症。结直肠癌是一种多因素疾病，涉及遗传、遗传、环境和生活方式等危险因素。大多数结直肠癌是散发性的，WNT、EGFR、P53、转化生长因子-β信号通路的突变顺序累积，APC、KRAS、BRAF和DNA错配修复基因被发现导致结直肠癌的发生和发展。除了这些遗传事件，详尽的转录分析显示，根据独特的克隆性、间质和免疫依赖性，结直肠癌的分子分类具有共识，有四种共识的分子亚型。这些共有的分子亚型概括了在结直肠癌中观察到的异质性，并预测了靶向治疗的反应。所有这些都极大地促进了对结直肠癌的诊断和治疗。然而，尤其是在晚期，由于缺乏早期诊断和有效的干预措施，结直肠癌变得难以治疗，导致转移，预后较差。这些糟糕的治疗结果突出表明，需要更好地了解导致结直肠癌启动、进展和扩散的机制。图片来源：https://doi.org/10.1186/s13046-023-02732-y 近日，来自中国科技大学的研究者们在J Exp Clin Cancer Res杂志上发表了题为“METTL16 promotes glycolytic metabolism reprogramming and colorectal cancer progression”的文章，该研究结果表明，METTL16/SOGA1/PDK4轴可能是结直肠癌有希望的治疗靶点。糖酵解是癌症的关键标志，并维持恶性肿瘤的发生和发展。N6-甲基腺苷(M6A)修饰在糖酵解中的作用在很大程度上是未知的。本研究探讨了M6A甲基转移酶METTL16在糖酵解代谢中的生物学作用，揭示了结直肠癌发生发展的新机制。研究者用生物信息学和免疫组织化学(IHC)方法评价METTL16的表达和预后价值。分析METTL16在体内和体外对结直肠癌进展的生物学作用。糖酵解代谢实验验证METTL16和自噬葡萄糖抑制因子(SOGA1)的生物学功能。通过蛋白质/RNA稳定性、RNA免疫沉淀(RIP)、共免疫沉淀(Co-IP)和RNA下拉实验，探讨了其可能的分子机制。 SOGA1是METTL16的直接下游靶点，参与METTL16介导的糖酵解和结直肠癌进展。METTL16通过结合“阅读器”蛋白胰岛素样生长因子2mRNA结合蛋白1(IGF2BP1)显著增强SOGA1的表达和mRNA的稳定性。随后，SOGA1促进AMPK复合体的泛素化，抑制AMPK的表达和磷酸化，从而上调控制糖代谢的关键蛋白丙酮酸脱氢酶激酶4(PDK4)。此外，阴阳1号(YY1)可通过直接与其启动子结合而转录抑制结直肠癌细胞中METTL16的表达。临床资料表明，METTL16的表达与SOGA1、PDK4呈正相关，与结直肠癌患者的预后不良有关。 METTL16促进的SOGA1 m6A修饰在CRC进展中的机制图图片来源: https://doi.org/10.1186/s13046-023-02732-y 本研究结果表明，METTL16在结直肠癌进展中具有促进肿瘤的作用。METTL16在结直肠癌组织中表达上调，与结直肠癌患者的预后不良有关。从机制上讲，METTL16/SOGA1/PDK4信号轴通过诱导糖酵解促进结直肠癌进展。这一发现为探索新的结直肠癌诊断生物标记物和治疗靶点提供了新的见解。（生物谷 Bioon.com）参考文献 Wei Wei et al. METTL16 promotes glycolytic metabolism reprogramming and colorectal cancer progression. J Exp Clin Cancer Res. 2023 Jun 20;42(1):151. doi: 10.1186/s13046-023-02732-y.

临床研究