新加坡南洋理工大學化學與生物醫學工程學院Chen Peng教授團隊在自然出版社與川大華西醫院生物治療國家重點實驗室聯合主辦的《Signal Transduction and Targeted Therapy》 （STTT）上發表研究性論文，發現血管緊張素II（AngII）受體的激活能促進白色脂肪棕色化，這個發現有可能為肥胖、糖尿病和相關代謝紊亂疾病提供新的治療策略（http://www.nature.com/ articles/sigtrans， 閱讀原文及下載PDF可直接點擊本文最下方“閱讀原文”）。Chen Peng教授是該文的通訊作者，Aung Than博士為第一作者。
四川大學賈大教授團隊在自然出版社與川大華西醫院生物治療國家重點實驗室聯合主辦的《Signal Transduction and Targeted Therapy》（STTT）上發表了研究性文章，該項研究成果利用生物化學、細胞生物學、結構生物學等手段確定了沙眼衣原體效應蛋白IncE與逆轉運復合體(retromer)復合體亞單位SNX5相互作用的分子機制，闡述了IncE抑制逆轉運復合體的運輸通路機制，深化了研究人員對病原細菌干擾宿主運輸通路機制的認識。
浙一醫院盛勤松博士和杭州師范大學醫學院鞠振宇教授團隊在自然出版社與川大華西醫院生物治療國家重點實驗室聯合主辦的《Signal Transduction and Targeted Therapy》（STTT）上發表了研究性文章，發現補充NAD+可改善小鼠的結腸退行性變。該文的通訊作者為盛勤松博士和鞠振宇教授，第一作者為朱栩棟博士。
美國德克薩斯大學安德森癌癥研究中心孫少聰教授在自然出版社與川大華西醫院生物治療國家重點實驗室聯合主辦的《Signal Transduction and Targeted Therapy》（STTT）上發表了綜述，討論NF-κB信號通路的活化與炎癥性疾病的關系，特別強調了以NF-κB抑制劑為基礎的免疫治療策略。該文的通訊作者為孫少聰教授，第一作者為劉婷博士。
美國麻省理工大學伍斯特理工學院Robert E. Dempski教授在自然出版社與川大華西醫院生物治療國家重點實驗室聯合主辦的《Signal Transduction and Targeted Therapy》（STTT）上發表了綜述，討論鋅轉運蛋白在細胞內穩態和在癌癥中的作用。該文的通訊作者為Robert E. Dempski教授，第一作者為Elizabeth Bafaro博士。
華西醫學二維碼
Cancerous inhibitor of protein phosphatase 2A (CIP2A), an endogenous protein phosphatase 2A (PP2A) inhibitor, has been identified as an oncoprotein in promoting cancer initiation and progression of several types of cancer. However, the expression and the role played by CIP2A in the pathogenesis of multiple myeloma (MM) remain unclear. In this study, we showed that CIP2A was overexpressed in human MM cell lines and MM patients’ bone marrow tissues. Clinicopathologic analysis showed that CIP2A expression was significantly correlated with clinical stage and percent of plasma cells in bone marrow. Kaplan–Meier analysis revealed that patients with high CIP2A expression presented with poorer overall survival rates than those with low CIP2A expression. Moreover, CIP2A knockdown in MM cells resulted in attenuated proliferative abilities. In addition, CIP2A depletion sensitizes dexamethasone (Dex)-resistant cells to Dex. The effect of CIP2A on proliferation and Dex therapy was mediated by the inhibition of PP2A, which in turn activated Akt. In vivo studies confirmed that CIP2A regulated MM tumorigenesis and the phosphorylation of Akt. Taken together, our results suggest that CIP2A oncoprotein plays an important role in MM progression and could serve as a prognosis marker and a novel therapeutic target for the treatment of patients with MM.
Retroviruses have helped shape the evolution of gene regulation, as highlighted by the mouse VL30-1 RNA that probably arose from a retrovirus infection. In a review article, Alan Garen from Yale University discusses the regulatory properties of VL30-1 RNA that control the expression of multiple genes, including those involved in cell proliferation and cancer. VL30-1 forms a complex with a tumor-suppressor protein called PSF that keeps tumor growth in check, inactivating PSF and promoting cell proliferation and cancer. VL30-1 RNA may have derived from a harmful genomic invader, but over evolutionary time it has co-opted the function of an endogenous regulatory RNA and become indispensable for normal mouse development and survival. Other RNAs that have a similar regulatory function as VL30-1 RNA exist in human cell.
Chemical agents that bind and reversibly modifyspecific DNA sequences could provide the foundation for safer anticancertreatments. Seeing that many current chemotherapy agents kill cancer cells byintroducing irreversible modifications at any site in the genome—damagingnon-target cells while also depleting the amount of drug available to fightcancer—Steven Rokita at the University of Maryland, along with colleagues inChina, sought a more selective and safer approach to treatment. They combinedDNA-modifying compounds known as quinone methides with nucleic acid constructsthat specifically bind particular gene sequences, allowing for targetedtreatment. Importantly, these chemical modifications are potentiallyreversible, minimizing the damage that occurs if the quinone methide-nucleicacid conjugates briefly bind the wrong DNA sequence. This could open doors forthe development of less toxic, targeted chemotherapies that are effective atlower doses