TONSL促进肺腺癌的进展,免疫逃脱和药物敏感性
Anru Liang1, Zuotao Wu1, Ting Zhuo2
1Department of Cardio-Thoracic Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, Guangxi, China.
概括
类似Tonsoku的DNA修复蛋白 (TONSL) 促进肺腺癌 (LUAD) 的进展和不良预后. 准TONSL可能为LUAD提供一种新的治疗策略,影响免疫逃逸和药物敏感性.
科学领域:
- 分子生物学分子生物学
- 癌症研究 癌症研究
- 遗传学 是一个遗传学.
背景情况:
- 类似tonsoku的DNA修复蛋白 (TONSL) 对于通过同源重组来修复DNA双链断裂至关重要.
- 肺腺癌 (LUAD) 中TONSL的过度表达与瘤发育和不良患者结局有关.
研究的目的:
- 调查TONSL作为LUAD预后标记物的作用.
- 在LUAD中探索TONSL表达,临床特征和瘤行为之间的关系.
- 评估TONSL对LUAD免疫逃逸和药物敏感性的影响.
主要方法:
- 对TCGA数据库进行预后价值和风险因素相关性的生物信息分析.
- 使用实时定量PCR和免疫组织化学验证TONSL表达的验证.
- 在功能性测定中,siRNA介导的TONSL在肺癌细胞中的敲除.
- 与TONSL表达水平相关的免疫逃逸和药物敏感性的分析.
主要成果:
- TONSL的上调与LUAD细胞的增多,迁移和入侵相关,预测预后不佳.
- TONSL过度表达与LUAD中增强的免疫逃生机制有关.
- 改变TONSL表达会影响LUAD细胞对化疗和向疗法的敏感性.
结论:
- TONSL是LUAD的验证的预后标志物,其高表达与预后不佳有关.
- TONSL上调有助于免疫逃避,并影响LUAD中的药物敏感性.
- TONSL代表了治疗肺腺癌的潜在新型治疗标.
更多相关视频
06:03Orthotopic Transplantation of Syngeneic Lung Adenocarcinoma Cells to Study PD-L1 Expression
Published on: January 19, 2019
16.9K
09:38Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib
Published on: June 26, 2019
7.9K
相关概念视频
Adaptive Mechanisms in Cancer Cells
5.7K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
5.7K
Tumor Progression
6.3K
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...
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...
6.3K
Treatment Resistant Cancers
3.3K
Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.3K
Metastasis
5.5K
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
5.5K
Targeted Cancer Therapies
7.5K
The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
There are several types of targeted therapies against...
7.5K
