长非编码RNACDKN2B-AS1促进肝细胞癌的进展通过E2F转录因子1/G蛋白子单元α Z轴
Zhi-Gang Tao1, Yu-Xiao Yuan2, Guo-Wei Wang3
1Department of Radiology, Hangzhou Cancer Hospital, Hangzhou 310000, Zhejiang Province, China.
World journal of gastrointestinal oncology
|December 11, 2023
概括
长非编码RNACDKN2B-AS1通过与E2F1相互作用来增加GNAZ转录,促进肝细胞癌 (HCC) 的进展. 这一发现为HCC治疗提供了潜在的治疗点.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 长非编码RNAs (lncRNAs) 与癌症生物学有关.
- lncRNA CDKN2B-AS1已与各种恶性瘤有关.
- 在肝细胞癌 (HCC) 中CDKN2B-AS1的特定作用需要进一步阐明.
研究的目的:
- 研究lncRNA CDKN2B-AS1在肝细胞癌 (HCC) 进展中的作用.
主要方法:
- 使用定量实时PCR测量CDKN2B-AS1在HCC中的表达.
- 细胞增殖,细胞循环和细胞亡使用CCK-8,EDU和流细胞计进行了评估.
- RNA免疫沉降,光酶记者测定和染色体免疫沉降证实了分子相互作用和转录调节.
主要成果:
- 发现CDKN2B-AS1在HCC组织中受到上调.
- CDKN2B-AS1的耗尽抑制了HCC细胞增殖,诱导细胞循环停止,并促进了细胞亡.
- CDKN2B-AS1与E2F1相互作用,促进E2F1与GNAZ促进体结合,并促进GNAZ转录.
结论:
- CDKN2B-AS1通过招募E2F1来增强GNAZ转录来促进HCC的进展.
- 这种机制突出了CDKN2B-AS1作为HCC的潜在治疗点.
更多相关视频
03:37Author Spotlight: Impact of Intergenic Interactions on Disease-Identifying Dark Biomarkers
Published on: March 1, 2024
763
09:27Analysis of Liver Microenvironment During Early Progression of Non-Alcoholic Fatty Liver Disease-Associated Hepatocellular Carcinoma in Zebrafish
Published on: April 1, 2021
3.5K
相关概念视频
lncRNA - Long Non-coding RNAs
8.6K
In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...
8.6K
MAPK Signaling Cascades
5.6K
Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
5.6K
Inhibition of Cdk Activity
4.8K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.8K
Cancer-Critical Genes II: Tumor Suppressor Genes
7.4K
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
7.4K
Negative Regulator Molecules
35.4K
Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
35.4K
Positive Regulator Molecules
5.5K
Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
5.5K
