相关实验视频

Updated: Sep 20, 2025

In vitro Organoid Culture of Primary Mouse Colon Tumors

In vitro Organoid Culture of Primary Mouse Colon Tumors

Published on: May 17, 2013

通过调节细胞质Ca2+度,SEC61G促进结直肠癌的进展

Satoshi Higuchi^1,2, Hajime Otsu¹, Takaaki Masuda³

¹Department of Surgery, Kyushu University Beppu Hospital, 4546 Tsurumibaru, Beppu, Oita, 874-0838, Japan.

Journal of gastroenterology

|May 25, 2025

概括

通过增加水平和激活EGFR信号,促进结直肠癌 (CRC),影响细胞循环的进展. 这突出了SEC61G作为CRC的潜在预后生物标志物和治疗点.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

细胞内 (Ca2+) 信号传递对癌症过程至关重要.
该SEC61复合体与从内细胞网膜的泄漏有关.
在结直肠癌 (CRC) 进展中,SEC61转位子玛子单元 (SEC61G) 的特定作用尚不清楚.

研究的目的:

研究SEC61G影响结直肠癌 (CRC) 进展的机制.
确定SEC61G作为预后生物标志物和CRC治疗标的潜力.

主要方法:

癌症基因组图谱数据集的生物信息学分析.
在CRC细胞和组织中通过RT-qPCR和免疫组织化学验证SEC61G表达.
在体外和体外实验评估SEC61G调制对CRC细胞增殖的影响.
对单细胞RNA测序 (scRNA-seq) 和空间转录组测序 (ST-seq) 数据的分析.

主要成果:

在CRC组织中,SEC61G显著上调,并与预后不佳有关.
SEC61G过度表达增强了CRC细胞的增殖,促进了细胞周期的进展 (G1到S阶段),并激活了EGFR通路.
SEC61G过度表达增加了细胞质Ca2+水平,通过calmodulin激活EGFR信号传递.
scRNA-seq和ST-seq数据证实瘤上皮细胞中较高的SEC61G表达,与EGFR通路基因共同表达.

结论:

SEC61G通过调节细胞质Ca2+,EGFR激活和细胞循环进展来促进CRC进展.
SEC61G代表了CRC的一个潜在的预后生物标志物.
SEC61G是结直肠癌的潜在治疗点.

关键词:

是一种结肠直肠癌是一种癌症.细胞内膜网膜 (ER) 是一个皮表皮肤生长因子受体 (EGFR)SEC61 转位子子单位玛 (SEC61G)

更多相关视频

Live Cell Calcium Imaging Combined with siRNA Mediated Gene Silencing Identifies Ca2+ Leak Channels in the ER Membrane and their Regulatory Mechanisms

Live Cell Calcium Imaging Combined with siRNA Mediated Gene Silencing Identifies Ca2+ Leak Channels in the ER Membrane and their Regulatory Mechanisms

Published on: July 7, 2011

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

相关概念视频

Feedback Regulation of Calcium Concentration

Feedback Regulation of Calcium Concentration

Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...

Calmodulin-dependent Signaling

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...

Tumor Progression

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...