胃肠道癌症中的六金酶:从分子洞察到治疗机会
Guodong Liang1, Yuehan Ma1, Ping Deng2
1First Surgery Department of Colorectal, Gastric, and Abdominal Tumors, Jilin Cancer Hospital, Changchun 130012, China.
Seminars in oncology
|June 5, 2025
概括
六催化酶 (HKs) 是癌症代谢和细胞死亡的关键. 抑制HKs显示了通过向亡和免疫逃避来治疗胃肠道癌症的前景.
科学领域:
- 生物化学 生化学
- 在瘤学瘤学.
- 分子生物学分子生物学
背景情况:
- 六基酶 (HKs) 是糖解中的关键酶,将葡萄糖转化为葡萄糖-6-酸盐.
- HKs的失调与胃肠道 (GI) 癌症的代谢变化和进展有关,包括胃,结直肠,食道和胰腺癌.
- HKs还在调节细胞死亡途径 (如自和亡) 中发挥非正规的作用.
研究的目的:
- 审查HKs在肠道癌症中的机制性参与.
- 探索HKs在糖溶性重编程,亡抵抗,自,免疫逃避,转移和药物耐药性中的作用.
- 突出 HKs 作为诊断和治疗目标的潜力.
主要方法:
- 对胃肠道癌症中赫索基因酶研究的文献综述.
- 分析HKs在代谢重编程和非代谢功能中的作用.
- 检查HKs在癌细胞死亡,免疫反应和耐药性的参与.
主要成果:
- 通过抑制亡和抑制免疫反应,HK2促进肝细胞癌 (HCC).
- 在HCC中HK2的表达减少了对自然杀手细胞细胞毒性的敏感性,帮助免疫逃生.
- 在HCC中,HKDC1与ACTA2的相互作用对STAT1信号传递和PD-L1表达至关重要.
- 黄海抑制剂3-BP通过引起内细胞网膜应激和氧化损伤,诱导HCC中的亡.
结论:
- 肝癌是肠胃癌的多方面的调节者,影响新陈代谢,细胞死亡和免疫逃逸.
- 针对HKs,例如3-BP,为肠道癌症提供了潜在的治疗策略.
- 对HKs作用的进一步研究可能会为这些恶性瘤带来新的诊断和治疗方法.
相关概念视频
Targeted Cancer Therapies
7.8K
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...
7.8K
Combination Therapies and Personalized Medicine
5.1K
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...
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...
5.1K
Inhibition of Cdk Activity
4.9K
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...
4.9K
Mitogens and the Cell Cycle
7.0K
Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
7.0K
Cancer-Critical Genes II: Tumor Suppressor Genes
8.2K
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...
8.2K
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists
267
Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy. SP binds and activates...
267


