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| 1 | Cancer metabolic reprogramming: importance, main features, and potentials for precise targeted anti-cancer therapies显示文摘Cancer cells are well documented to rewire their metabolism and energy production networks to support and enable rapid proliferation, continuous growth, survival in harsh conditions, invasion, metastasis, and resistance to cancer treatments. Since Dr. Otto Warburg's discovery about altered cancer cell metabolism in 1930, thousands of studies have shed light on various aspects of cancer metabolism with a common goal to find new ways for effectively eliminating tumor cells by targeting their energy metabolism. This review highlights the importance of the main features of cancer metabolism, summarizes recent remarkable advances in this field, and points out the potentials to translate these scientific findings into life-saving diagnosis and therapies to help cancer patients. | Liem Minh Phan Sai-Ching Jim Yeung Mong-Hong Lee | 2014 | Cancer Biology & Medicine2014，11，1： | 11 |
| 2 | Impact of diabetes on promoting the growth of breast cancer显示文摘Background:Type Ⅱ diabetes mellitus(DM2)is a significant risk factor for cancers,including breast cancer.However,a proper diabetic breast cancer mouse model is notwell-established for treatment strategy design.Additionally,the precise diabetic signaling pathways that regulate cancer growth remain unresolved.In the present study,we established a suitable mouse model and demonstrated the pathogenic role of diabetes on breast cancer progression.Methods:We successfully generated a transgenic mouse model of human epidermal growth factor receptor 2 positive(Her2^(+) or ERBB2)breast cancer with DM2 by crossing leptin receptor mutant(Lepr^(db/+))mice with (MMTV-ErbB2/neu)mice.Themousemodelswere administrated with antidiabetic drugs to assess the impacts of controlling DM2 in affecting tumor growth.Magnetic resonance spectroscopic imaging was employed to analyze the tumor metabolism.Results:Treatment with metformin/rosiglitazone in MMTV-ErbB2/Lepr^(db/db) mousemodel reduced serum insulin levels,prolonged overall survival,decreased cumulative tumor incidence,and inhibited tumor progression.Anti-insulin resistance medications also inhibited glycolytic metabolism in tumors in vivo as indicated by the reduced metabolic flux of hyperpolarized ^(13)C pyruvate-to-lactate reaction.The tumor cells from MMTV-ErbB2/Lepr^(db/db) transgenic mice treated with metformin had reprogrammed metabolism by reducing levels of both oxygen consumption and lactate production.Metformin decreased the expression of Myc and pyruvate kinase isozyme 2(PKM2),leading to metabolism reprogramming.Moreover,metformin attenuated the mTOR/AKT signaling pathway and altered adipokine profiles.Conclusions:MMTV-ErbB2/Lepr^(db/db) mouse model was able to recapitulate diabetic HER2^(+) human breast cancer.Additionally,our results defined the signaling pathways deregulated in HER2^(+) breast cancer under diabetic condition,which can be intervened by anti-insulin resistance therapy. | Ping-Chieh Chou Hyun Ho Choi Yizhi Huang Enrique Fuentes-Mattei Guermarie Velazquez-Torres Fanmao Zhang Liem Phan Jaehyuk Lee Yanxia Shi James A.Bankson Yun Wu Huamin Wang Ruiying Zhao Sai-Ching Jim Yeung Mong-Hong Lee | 2021 | Cancer Communications2021，41，5： | 4 |
| 3 | Farmer's participation in rice variety selection显示文摘 | TRUONG THI NGOC CHI PHAN VAN LIEM THELMA PARIS | 2007 | Omonrice2007，15，： | 1 |
| 4 | 糖尿病对促进乳腺癌生长的影响显示文摘背景与目的2型糖尿病(typeⅡdiabetes mellitus,DM2)是包括乳腺癌在内的多种癌症的危险因素。目前,尚未建立可用于研究的糖尿病乳腺癌小鼠模型。另外,调节癌症生长的糖尿病信号通路也尚未明确。在本研究中,我们建立了一个糖尿病乳腺癌小鼠模型,并证实了糖尿病在乳腺癌进展中的影响。方法通过将瘦素受体突变(Lepr^(db/+))小鼠和MMTV-ErbB2/neu小鼠杂交,成功构建了人表皮生长因子受体2阳性(human epidermal growth factor receptor 2,Her2^(+)或ERBB2)的乳腺癌转基因小鼠模型。用抗糖尿病药物治疗该小鼠模型来评价治疗DM2对肿瘤生长的影响。用磁共振波谱成像分析肿瘤代谢情况。结果用二甲双胍/罗格列酮治疗MMTV-ErbB2/Lepr^(db/db)小鼠模型可降低血清胰岛素水平,延长生存,降低肿瘤累积发生率,抑制肿瘤进展。超极化^(13)C标记的丙酮酸/乳酸转换代谢流降低,表明抗胰岛素抵抗治疗抑制了体内实验中肿瘤糖酵解。用二甲双胍处理MMTV-ErbB2/Lepr^(db/db)转基因小鼠来源的肿瘤细胞,降低了耗氧量和乳酸产量,使细胞代谢发生了重新编程。二甲双胍可降低Myc和丙酮酸激酶M2型同工酶(pyruvate kinase isozyme 2,PKM2)的表达,引起代谢重编程。另外,二甲双胍可阻断mTOR/AKT信号通路并改变脂肪因子谱。结论MMTV-ErbB2/Lepr^(db/db)转基因小鼠模型可用于糖尿病HER2^(+)人乳腺癌的研究。本研究明确了糖尿病状态下HER2^(+)人乳腺癌中失调的信号通路,该通路可被抗胰岛素抵抗治疗干预。 | Ping-Chieh Chou Hyun Ho Choi Yizhi Huang Enrique Fuentes-Mattei Guermarie Velazquez-Torres Fanmao Zhang Liem Phan Jaehyuk Lee Yanxia Shi James A.Bankson Yun Wu Huamin Wang Ruiying Zhao Sai-Ching Jim Yeung Mong-Hong Lee | 2022 | 癌症2022，41，3： | 0 |
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