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首页> 外文期刊>Journal of Cachexia, Sarcopenia and Muscle >Ursodeoxycholic acid and its emerging role in attenuation of tumor growth in gastrointestinal malignancies
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Ursodeoxycholic acid and its emerging role in attenuation of tumor growth in gastrointestinal malignancies

机译：熊去氧胆酸及其在胃肠道恶性肿瘤中减缓肿瘤生长的新作用

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Dear Editor,;I read with great interest the recent article by Tschirner et al. [1]. Interestingly, recent data suggest that ursodeoxycholic acid (UDCA) may attenuate tumor growth in a number of gastrointestinal malignancies.;For instance, tauro-ursodeoxycholic acid when administered along with celecoxib attenuates proliferation and tumor growth in colonic adenomas [2]. Interestingly, UDCA decreases the odds of advanced lesions in males only [3]. Similarly, UDCA downregulates c-Myc expression [4]. As a result, it attenuates tumor growth in colon carcinomas. CDK6 expression is also decreased secondary to UDCA administration. UDCA downregulates Cox-2 also, thus further inhibiting tumor growth. It also attenuates CCAAT/enhancer binding protein beta (C/EBPbeta) at the same time [5]. It also effects p38 and Ras expression and thereby further modulates Cox-2 function. Recently, UDCA conjugates with glutamic acid have been developed that result in enhanced intraluminal delivery of UDCA inside the colon [6].;Similarly, UDCA inhibits gastric carcinogenesis. It does this by modulating the MEK/ERK pathway. It accentuates MEK1/2 phosphorylation as well as ERK1/2 phosphorylation [7]. DR 5 receptors are necessary for UDCA-mediated apoptosis. Modulation of the raft formation/ROS production/PKCδ activation pathway can effect UDCA-mediated apoptosis as it in turn effects and controls DR5 expression [8]. Apoptosis secondary to UDCA is attenuated by U0126 as well as by PD98059.;Similarly, DLC1 degradation by proteosomes is attenuated by UDCA [9]. Subsequently, there is decreased proliferation and growth in hepatocellular carcinomas. UDCA administration is simultaneously accompanied by a decrease in RhoA activity. Similarly, UDCA upregulates Bax expression and downregulates Bcl-2 expression. Interestingly, the p53-caspase 8 pathway is activated by UDCA which mediates the conversion from oxaliplatin-induced necrosis to apoptosis in hepatocellular carcinomas [10]. At the same time, UDCA inhibits ROS production. Hence, combination therapy in hepatocellular carcinomas may benefit from the addition of UDCA. Similarly, UDCA has a negative impact on the incidence rate of cholangiocarcinomas in patients with primary sclerosing cholangitis [11].;It is clearly evident from the above examples that UDCA can play a major role in attenuating carcinogenesis in the gastrointestinal tract. There is a clear and urgent need for further studies in this regard.;The author has no conflicts of interest.
机译：亲爱的编辑：我非常感兴趣地阅读了Tschirner等人的最新文章。 [1]。有趣的是，最近的数据表明，熊去氧胆酸（UDCA）可能会减轻许多胃肠道恶性肿瘤的生长;例如，牛磺-熊去氧胆酸与塞来昔布同时给药可减弱结肠腺瘤的增殖和肿瘤生长[2]。有趣的是，UDCA仅降低了男性晚期病变的几率[3]。同样，UDCA下调c-Myc表达[4]。结果，它减弱了结肠癌中的肿瘤生长。继UDCA施用后，CDK6表达也降低。 UDCA还下调Cox-2，从而进一步抑制肿瘤生长。它还同时减弱了CCAAT /增强子结合蛋白β（C / EBPbeta）[5]。它还影响p38和Ras表达，从而进一步调节Cox-2功能。最近，已经开发了UDCA与谷氨酸的结合物，其导致结肠内UDCA的腔内递送增强[6]。类似地，UDCA抑制胃癌发生。它通过调节MEK / ERK途径来做到这一点。它增强了MEK1 / 2的磷酸化以及ERK1 / 2的磷酸化[7]。 DR 5受体是UDCA介导的细胞凋亡所必需的。筏形成/ ROS产生/PKCδ激活途径的调节可影响UDCA介导的细胞凋亡，因为它进而影响并控制DR5表达[8]。 U0126和PD98059减弱了UDCA继发的凋亡;类似地，UDCA减弱了蛋白体对DLC1的降解[9]。随后，肝细胞癌的增殖和生长减少。 UDCA给药同时伴随RhoA活性降低。同样，UDCA上调Bax表达，下调Bcl-2表达。有趣的是，UDCA激活了p53-caspase 8通路，该通路介导了奥沙利铂诱导的坏死向肝细胞癌凋亡的转化[10]。同时，UDCA抑制ROS的产生。因此，肝细胞癌的联合治疗可受益于UDCA的添加。同样，UDCA对原发性硬化性胆管炎患者的胆管癌的发生率也有负面影响[11]。从以上示例可以清楚地看出，UDCA在减缓胃肠道癌变中起主要作用。在这方面显然有迫切需要进一步的研究。作者没有利益冲突。

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