Cell:高脂肪饮食可加速诱发结直肠癌

2019-02-24 顾然 生物探索

近年来,虽然癌症死亡率在整体下降,但是医生们却注意到一个可怕的反常现象:55岁以下人群因结直肠癌死亡的人数似乎在逐渐攀升。根据美国癌症协会的数据,2007年至2016年间,这一疾病年轻群体的死亡人数增加了1%。

近年来,虽然癌症死亡率在整体下降,但是医生们却注意到一个可怕的反常现象:55岁以下人群因直肠癌死亡的人数似乎在逐渐攀升。根据美国癌症协会的数据,2007年至2016年间,这一疾病年轻群体的死亡人数增加了1%。

是什么原因导致直肠癌死亡率不降反升?近日,由Salk研究所的科学家们领导的一项新研究或许给出了答案:高脂肪饮食扰乱了肠道胆汁酸的平衡,并触发荷尔蒙信号,从而促进了结肠直肠癌的生长。

它解释了,在一个脂肪含量较高的饮食普遍存在的时代,为什么需要几十年才能发展成的结直肠癌却出现在年轻人身上。研究结果于2019年2月21日发表在《Cell》杂志上。

“这项研究提供了一种降低炎症、恢复肠道健康和显著减少肿瘤进展的新方法。” 霍华德休斯医学研究所基因表达实验室主任、Salk研究所发育生物学主席Ronald Evans教授说道。

结直肠癌发生机制

大肠和小肠(通常被统称为“肠道”)是辛勤工作的器官。当你吃东西的时候,你的肠道需要不断地再生它的内壁,以消除消化酸造成的伤害。为了做到这一点,肠道中储存了大量的干细胞,当需要的时候,这些干细胞可以补充内壁细胞。

科学家们发现,结肠直肠癌往往源于这些干细胞的突变。最常见的结直肠癌相关突变发生在一种叫做APC的基因中,这种基因通常起着“抑癌”基因的作用,因为它控制着细胞分裂的频率。APC基因的突变可以消除这种控制,使细胞迅速分裂并发生癌变。

我们肠道中“漂浮”着30种胆汁酸,帮助消化食物、吸收胆固醇、脂肪和脂溶性营养素。在过去的四十年中,Evans和他的同事研究了胆汁酸的作用。该实验室发现,胆汁酸通过一种名为Farnesoid (FXR)的蛋白质向肠道干细胞发送激素信号。

研究的第一作者、Salk大学博士后傅婷(Ting Fu,音译)从APC突变小鼠模型的线索入手。这些小鼠出现了结肠直肠癌的早期信号,因此她决定同时监测小鼠胆汁酸水平。结果发现,已知与FXR相互作用的胆汁酸的种类在癌症发生的同时增加了,而且额外胆汁酸的存在加速了癌症的进展。

“我们发现,癌症的增长与胆汁酸密切相关,”Salk的资深科学家、该研究的共同通讯作者Michael Downes说,“我们的实验表明,保持胆汁酸的平衡是减少癌症生长的关键。”

高脂肪饮食火上浇油

进一步研究发现,给这些小鼠喂食高脂肪的食物就像是火上浇油。

高脂肪的食物会增加两种特定胆汁酸的含量,这两种胆汁酸会抑制FXR的活性。肠道想要自我修复,FXR会使这一修复过程缓慢、稳定和安全地进行。当胆汁酸抑制FXR时,一些干细胞就开始快速生长并积累DNA损伤。



当fxr调控的基因网络被特定的胆汁酸或高脂肪饮食破坏时,结肠癌的生长(用绿色显示的分裂细胞数量来衡量)会显著增加。图片来源:Salk Institute

“我们知道高脂肪饮食和胆汁酸都是导致癌症的危险因素,但我们没想到它们会同时影响肠道干细胞中的FXR。” 研究人员说道。

有APC突变的小鼠出现了良性的腺瘤。在人类中,腺瘤常见于肠道,通常在结肠镜检查时切除。这些增生通常需要几十年的时间才会转化为恶性腺癌。然而,当喂食高脂肪食物时,这些小鼠的腺瘤很快就会癌变。

这或许就解释了,为什么年轻人中结肠直肠癌死亡率的上升。随着高脂肪饮食在美国变得越来越普遍,越来越多的APC突变患者通过这些饮食加速了癌症的生长。

潜在的新抗癌武器

既然弄明白了癌症加速生长的原因,那能否根据这一细胞机制,找到新的抗癌武器呢?研究人员做了尝试。他们使用了一种名为FexD的分子来激活肠道干细胞中的FXR。FexD似乎可以抵消小鼠器官模型和人类结肠癌细胞系中不平衡胆汁酸造成的损害。

研究小组也强调,在FexD用于人体试验之前还需要进行更多的实验,但这种候选药物很有潜力:它可以到达结肠,而且只对FXR起作用,因此它产生的副作用应该比其他药物更少。

虽然结肠癌被认为是无法治愈的,但这项研究或许为理解和治疗结肠癌开辟了一个全新的领域。

原始出处:
Ting Fu, Sally Coulter, Eiji Yoshihara, et al. FXR Regulates Intestinal Cancer Stem Cell Proliferation. Cell. Feb 2019.

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    2019-02-25 维他命
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    2019-02-26 pcw111

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