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AUTOPHAGY：自噬促进肿瘤代谢重编程

2018-07-03 海北 MedSci原创

自噬代谢肿瘤
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尽管我们对巨自噬/自噬的促存活作用有了一定的了解，但是由于自噬受损引起的营养缺乏如何影响致癌KRAS驱动的肿瘤进展却知之甚少。

基底自噬的缺陷限制了细胞内成分再循环的营养供应。尽管我们对巨自噬/自噬的促存活作用有了一定的了解，但是由于自噬受损引起的营养缺乏如何影响致癌KRAS驱动的肿瘤进展却知之甚少。
最近，来自美国的研究人员证明，自噬基因Atg5的条件性敲除（atg5-KO）将KRASG12V驱动的荷瘤小鼠的存活延长了38％。尽管发病较快，但atg5-KO肿瘤在晚期肿瘤发生过程中传播较慢。 atg5-KO肿瘤细胞显示出线粒体功能降低和线粒体断裂增加。
尽管ASNS（天冬酰胺合成酶），天然天冬酰胺合成的关键酶，出现了补偿性过表达，代谢物谱显示非必需氨基酸天冬酰胺出现了缺乏。自噬或ASNS的抑制减少了KRASG12V驱动的肿瘤细胞增殖，迁移和侵袭，其可以通过天冬酰胺补充或敲除MFF（线粒体裂变因子）来挽救。
最后，这些观察结果反映在人类癌症衍生数据中，将ASNS过度表达与多种癌症的不良临床结果联系起来。
总之，该数据记录了通过自噬和ASNS调控的广泛但特异性的天冬酰胺稳态，突出了先前未被认识的自噬在恶性KRAS驱动的肿瘤进展中的作用。

原始出处：
H. Helen Lin et al. Autophagic Reliance Promotes Metabolic Reprogramming in Oncogenic KRAS-driven Tumorigenesis. AUTOPHAGY 2018, DOI: https://doi.org/10.1080/15548627.2018.1450708

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    2018-07-04 sunfeifeiyang

    学习

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    2018-07-04 神功盖世

    学习

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    2018-07-04 jihuaijun1112

    学习学习学习

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  4. 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time=2018-07-03, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=328916, encodeId=536c3289168f, content=学习谢谢分享, beContent=null, objectType=article, channel=null, level=null, likeNumber=59, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=https://wx.qlogo.cn/mmopen/mStl88fu4Nd44v3xHnnictn9UpctwtH62EPQ59TMdI9lnqHMgQ16nH7GmGCfpzicsHgjibYVk6vwSpXrC86gMibRkoaIzf5HwSz7/0, createdBy=78cc1691107, createdName=龙胆草, createdTime=Tue Jul 03 08:08:35 CST 2018, time=2018-07-03, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=328909, encodeId=c05932890956, content=学习了谢谢, beContent=null, objectType=article, channel=null, level=null, likeNumber=80, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=http://thirdwx.qlogo.cn/mmopen/vi_32/Q0j4TwGTfTLbTp9nZtjwVrSZNxAXbAicnKQWnic2eBdJUQYhxO36XdkstSicr7FVF8p5ReH4omtmsbnLdvZLiaJJ1A/132, 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createdName=zb1235672, createdTime=Tue Jul 03 07:18:30 CST 2018, time=2018-07-03, status=1, ipAttribution=)]
    2018-07-03 神功盖世

    阅

    0

  5. 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createdName=zb1235672, createdTime=Tue Jul 03 07:18:30 CST 2018, time=2018-07-03, status=1, ipAttribution=)]
    2018-07-03 apple57298871

    好

    0

  6. 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createdName=zb1235672, createdTime=Tue Jul 03 07:18:30 CST 2018, time=2018-07-03, status=1, ipAttribution=)]
    2018-07-03 衣带渐宽

    学习

    0

  7. 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createdBy=8bff2327056, createdName=kafei, createdTime=Tue Jul 03 07:37:12 CST 2018, time=2018-07-03, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=328905, encodeId=de9e3289052a, content=优质资源.共同学习, beContent=null, objectType=article, channel=null, level=null, likeNumber=68, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=https://wx.qlogo.cn/mmopen/oLAjfB7s1ib06iaV3D9Tg5K0LqDY57Aia0TOQByoJhNt3icm4sfukp500hLH6RHOpFdV01NbECtAV7s0qKpQPibyRukQAwAmqJU3X/0, createdBy=f91f1928792, createdName=九九消寒, createdTime=Tue Jul 03 07:27:46 CST 2018, time=2018-07-03, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=328891, encodeId=22163288917a, content=学习了!!!!!, beContent=null, objectType=article, channel=null, level=null, likeNumber=65, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=, createdBy=59321624668, createdName=zb1235672, createdTime=Tue Jul 03 07:18:30 CST 2018, time=2018-07-03, status=1, ipAttribution=)]
    2018-07-03 龙胆草

    学习谢谢分享

    0

  8. 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createdBy=8bff2327056, createdName=kafei, createdTime=Tue Jul 03 07:37:12 CST 2018, time=2018-07-03, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=328905, encodeId=de9e3289052a, content=优质资源.共同学习, beContent=null, objectType=article, channel=null, level=null, likeNumber=68, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=https://wx.qlogo.cn/mmopen/oLAjfB7s1ib06iaV3D9Tg5K0LqDY57Aia0TOQByoJhNt3icm4sfukp500hLH6RHOpFdV01NbECtAV7s0qKpQPibyRukQAwAmqJU3X/0, createdBy=f91f1928792, createdName=九九消寒, createdTime=Tue Jul 03 07:27:46 CST 2018, time=2018-07-03, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=328891, encodeId=22163288917a, content=学习了!!!!!, beContent=null, objectType=article, channel=null, level=null, likeNumber=65, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=, createdBy=59321624668, createdName=zb1235672, createdTime=Tue Jul 03 07:18:30 CST 2018, time=2018-07-03, status=1, ipAttribution=)]
    2018-07-03 kafei

    学习了谢谢

    0

  9. 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createdBy=8bff2327056, createdName=kafei, createdTime=Tue Jul 03 07:37:12 CST 2018, time=2018-07-03, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=328905, encodeId=de9e3289052a, content=优质资源.共同学习, beContent=null, objectType=article, channel=null, level=null, likeNumber=68, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=https://wx.qlogo.cn/mmopen/oLAjfB7s1ib06iaV3D9Tg5K0LqDY57Aia0TOQByoJhNt3icm4sfukp500hLH6RHOpFdV01NbECtAV7s0qKpQPibyRukQAwAmqJU3X/0, createdBy=f91f1928792, createdName=九九消寒, createdTime=Tue Jul 03 07:27:46 CST 2018, time=2018-07-03, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=328891, encodeId=22163288917a, content=学习了!!!!!, beContent=null, objectType=article, channel=null, level=null, likeNumber=65, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=, createdBy=59321624668, createdName=zb1235672, createdTime=Tue Jul 03 07:18:30 CST 2018, time=2018-07-03, status=1, ipAttribution=)]
    2018-07-03 九九消寒

    优质资源.共同学习

    0

  10. 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createdBy=8bff2327056, createdName=kafei, createdTime=Tue Jul 03 07:37:12 CST 2018, time=2018-07-03, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=328905, encodeId=de9e3289052a, content=优质资源.共同学习, beContent=null, objectType=article, channel=null, level=null, likeNumber=68, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=https://wx.qlogo.cn/mmopen/oLAjfB7s1ib06iaV3D9Tg5K0LqDY57Aia0TOQByoJhNt3icm4sfukp500hLH6RHOpFdV01NbECtAV7s0qKpQPibyRukQAwAmqJU3X/0, createdBy=f91f1928792, createdName=九九消寒, createdTime=Tue Jul 03 07:27:46 CST 2018, time=2018-07-03, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=328891, encodeId=22163288917a, content=学习了!!!!!, beContent=null, objectType=article, channel=null, level=null, likeNumber=65, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=, createdBy=59321624668, createdName=zb1235672, createdTime=Tue Jul 03 07:18:30 CST 2018, time=2018-07-03, status=1, ipAttribution=)]
    2018-07-03 zb1235672

    学习了!!!!!

    0

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牙齿支持组织中的血管生成改变在牙周炎中起重要作用。间充质干细胞（MSC）可以通过旁分泌功能影响内皮细胞（EC）的血管形成。据报道，自噬与细胞分泌密切相关。

Diabetes：IL-6可通过将自噬与抗氧化反应相偶联从而减少β细胞氧化应激损伤

活性氧（ROS）产生是糖尿病β细胞功能障碍的关键因素。既往研究表明，多效性的细胞因子IL-6与β细胞自噬相关，但IL-6是否影响β细胞的氧化应激尚不明确。Michelle R. Marasco等人利用糖尿病小鼠模型、体外培养的人类胰岛和啮齿动物的β细胞来研究IL-6是否影响氧化应激反应。结果显示IL-6偶联自噬抗氧化应激，可减少β细胞和人类胰岛的ROS。在活体内，β细胞特异性丧失IL-6信号使小鼠

AUTOPHAGY：自噬缺陷诱导骨流失

在最近的一项研究中，来自西安交通大学的研究人员使用成骨细胞特异性Atg7（自噬相关7）条件性敲除（cKO）小鼠研究了ATG7在体内发育和重塑阶段的直接作用。

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