相关实验视频

Updated: Jul 20, 2025

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure

Published on: August 11, 2017

通过 bergenin 降解幸存者,克服了 pemetrexed 的耐药性

Xiaoying Li^1,2, Qi Liang^1,2, Li Zhou³

¹Department of Radiology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, 410013, People's Republic of China.

Cellular oncology (Dordrecht, Netherlands)

|August 4, 2023

概括

贝尔根因有效地向生存素 (与癌症生长相关的蛋白质),以抑制非小细胞肺癌 (NSCLC) 的进展和化学抵抗. 这项研究突出了伯根因作为NSCLC治疗的有前途的治疗剂.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
癌症研究癌症研究

背景情况:

化学抵抗在非小细胞肺癌 (NSCLC) 中显著导致治疗失败和复发.
幸存者,一种瘤蛋白质,在恶性瘤中经常过度表达,并与预后不佳有关,但其在NSCLC致癌和化学抵抗中的确切作用需要进一步阐明.
开发针对生存表达的有效抑制剂对于改善NSCLC治疗结果至关重要.

研究的目的:

研究survivin在非小细胞肺癌 (NSCLC) 中的原始原始作用.
评估 bergenin 在 NSCLC 中的抗瘤活性和潜在机制.
为了确定贝根因能否克服NSCLC中的化学抵抗.

主要方法:

用MTS和殖民地形成试验来评估细胞增殖.
通过免疫块和免疫组织化学分析幸存者的表达和信号通路变化.
用异种移植模型在体外和体内评估了抗瘤效应.

主要成果:

发现Survivin在NSCLC组织中得到了上调,其耗尽抑制了瘤发生.
贝尔根因在体外和体内NSCLC模型中表现出显著的抗瘤作用.
贝尔根因通过Akt/Wee1/CDK1通路通过降低幸存者的调节来抑制细胞增殖和诱导细胞亡,导致幸存者的降解增加.
贝尔根因使NSCLC细胞对佩米特雷克斯重新敏感,增强化疗抵抗力.

结论:

幸存者的过度表达对于维持NSCLC细胞的恶性特征至关重要.
贝尔根因通过向幸存者,对抗NSCLC表现出强大的抗瘤活性.
伯根因代表了NSCLC治疗的有前途的治疗候选者,特别是在克服化疗抵抗方面.

关键词:

在BergeninBergenin里面化学抗药性化学抗药性是一种抗药性.非小细胞肺癌是非小细胞肺癌.幸存下来就是生存.在Ubiquitination中使用.

更多相关视频

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo

Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo

Published on: February 6, 2015

相关概念视频

Treatment Resistant Cancers

Treatment Resistant Cancers

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...

Long-patch Base Excision Repair

Long-patch Base Excision Repair

Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:

Abnormal Proliferation

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...

Targeted Cancer Therapies

Targeted Cancer Therapies

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...

Base Excision Repair

Base Excision Repair

One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
The first step of...

Combination Therapies and Personalized Medicine

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...