15。两种药物均可诱导4种细胞凋亡,两药联用可使BT-474、SK-BR-3和MDA-MB-231细胞凋亡率显著增加,P<0.01。实时荧光定量PCR与蛋白质印迹法检测结果发现,单独用药能上调Bax及下调Bcl-2基因表达水平,并下调p-Akt蛋白表达水平,其中BT-474、SK-BR-3和MDA-MB-231细胞的联合用药组效果更显著,P
胃癌是全球第三大致死率的恶性肿瘤,在确诊时往往处于疾病中晚期阶段。目前许多研究均提示胃癌患者体细胞基因组存在异常。然而,尽管目前胃癌基因组学特性方面取得很多进展,但病人预后并无明显改善。对于进展期/晚期胃癌(advanced

Buparlisib半抑制浓度 gastric cancer,AGC)患者,中位生存时间仅维持在12个月左右。曲妥珠单抗、雷莫芦单抗(ramucirumab)、阿帕替尼(apatinib)等的出现显示出胃癌分子靶向治疗的希望及针对肿瘤分子生物靶向治疗的重要性。本文就目前AGC分子靶向治疗的研究现状简要综述。
膜结合蛋白SH3GL1参与调控某些肿瘤细胞生物学行为,而其对紫杉醇耐药乳腺癌细胞的恶性生物学行为影响尚未见报道.为阐明SH3GL1对紫杉醇耐药敏感性的影响以及潜在的分子机制,本研究首先采用免疫组化法证实SH3GL1在紫杉醇耐药乳腺癌组织高表达(P<0.05);同时抑制SH3GL1表达(P<0.05),耐药基因MDR1表达降低(P<0.05),p-AKT和p-gp水平下降(P<0.05).上述结果表明,降低SH3GL1表达可以减弱紫杉醇耐药性,增加乳腺癌对紫杉醇的敏感性,这为临床上紫杉醇耐药乳腺癌患者的治疗提供了新的靶点.
Colon cancers develop adaptive mechanisms to survive under extreme conditions and 也许 display hallmarks ofunlimited proliferation and resistance to cell death. The deregulation of cell death is a key factor that contri-butes to chemoresistance in tumors. In a physiological context, balance between cell proliferation and death, and protection against cell damage are fundamental processes for maintaining gut epithelial homeostasis. The

mechanisms underlying anti-death cytoprotection and tumor resistance often bear common pathways, and although distinguishing them would be a challenge, it would also provide an opportunity to develop

advanced anti-cancer therapeutics. This review will outline cell death pathways(i.e., apoptosis, necrosis, and necroptosis), and discuss cytoprotective strategies in normal intestinal epithelium and death resistance mechanisms of colon tumor. In colorectal cancers, the intracellular mechanisms of death resistance include the direct alteration of apoptotic and necroptotic machinery and the upstream events modulating death effectors such as tumor suppressor gene inactivation and pro-survival signaling pathways. The autocrine, paracrine and exogenous factors 不 within a tumor microenvironment can also instigate resistance against apoptotic and necroptotic cell death in colon cancers through changes in receptor signaling or transporter uptake. The roles of cyclooxygenase-2/prostaglandin E2, growth factors, glucose, and bacterial lipopolysaccharides in colorectal cancer will be highlighted. Targeting anti-death pathways in the colon cancer tissue might be a promising approach outside of anti-proliferation and anti-angiogenesis strategies for developing novel drugs to treat refractory tumors.