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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Heat-shock protein 27 plays the key role in gemcitabine-resistance of pancreatic cancer cells.
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Heat-shock protein 27 plays the key role in gemcitabine-resistance of pancreatic cancer cells.

机译：热休克蛋白27在胰腺癌细胞的吉西他滨耐药中起关键作用。

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摘要

Pancreatic cancer is one of the most fatal types of cancer in developed countries. Most patients have locally advanced or metastatic cancerous lesions when they are diagnosed, due to the progressive, invasive and metastatic capacity of this disease to liver, lymph nodes and distant organs during early stages. Although the only curative therapy is complete surgical resection, the disease has usually already progressed by the time of diagnosis, and the majority of patients have metastatic disease. Therefore, palliative chemotherapy remains the only therapy for patients with progressive disease. Gemcitabine has been used for pancreatic cancer as the most effective anticancer drug. However, there are many cases resistant to gemcitabine. Thus, a better understanding of the molecular mechanisms of resistance to gemcitabine is essential to allow it to be used more effectively. Our previous proteomic studies demonstrated that the expression of heat-shock protein 27 (HSP27) was increased in gemcitabine-resistant pancreatic cancer cells and this might play a role in determining the sensitivity of pancreatic cancer to gemcitabine. Increased HSP27 expression in tumor specimens was related to resistance to gemcitabine and a shorter survival period in patients with pancreatic cancer. Furthermore, it has been shown that treatment strategies combining the HSP inhibitor KNK437 or interferon-γ (IFN-γ) with gemcitabine, were effective in gemcitabine-resistant pancreatic cancer cells in vitro. Furthermore, combined therapy of gemcitabine with IFN-γ of gemcitabine-resistant pancreatic cancer-bearing nude mice showed synergistic therapeutic effects on gemcitabine-resistant pancreatic cancer bearers. In this review, we summarize the current understanding of HSP27 and its role in gemcitabine resistance.
机译：胰腺癌是发达国家中最致命的癌症之一。大多数患者在被诊断出时具有局部晚期或转移性癌病灶，这是由于该疾病在早期对肝脏，淋巴结和远处器官具有渐进，侵袭和转移能力。尽管唯一的治疗方法是完全手术切除，但该疾病通常在诊断时就已经进展，大多数患者患有转移性疾病。因此，姑息化疗仍然是进行性疾病患者的唯一疗法。吉西他滨已作为最有效的抗癌药物用于胰腺癌。但是，有许多情况对吉西他滨有抗药性。因此，更好地理解对吉西他滨耐药的分子机制对于使其更有效地使用至关重要。我们以前的蛋白质组学研究表明，抗吉西他滨的胰腺癌细胞中热休克蛋白27（HSP27）的表达增加，这可能在确定胰腺癌对吉西他滨的敏感性中起作用。肿瘤标本中HSP27表达的增加与吉西他滨的耐药性以及胰腺癌患者的生存期缩短有关。此外，已经表明，结合HSP抑制剂KNK437或干扰素-γ（IFN-γ）与吉西他滨的治疗策略在体外对吉西他滨耐药的胰腺癌细胞有效。此外，吉西他滨与耐吉西他滨的胰腺癌裸鼠的IFN-γ联合治疗对耐吉西他滨的胰腺癌载体显示协同治疗作用。在这篇综述中，我们总结了对HSP27的当前了解及其在吉西他滨耐药中的作用。

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