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J Thorac Oncol. 2019 Jan;14(1):99-106. doi: 10.1016/j.jtho.2018.09.004. Epub 2018 Sep 18.
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PI3k/AKT signaling pathway: Erythropoiesis and beyond.PI3k/AKT 信号通路:红细胞生成及其他。
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Effects and mechanisms of betulinic acid on improving EGFR TKI-resistance of lung cancer cells.白桦脂酸对改善肺癌细胞 EGFR TKI 耐药性的作用及机制。
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Haspin: a promising target for the design of inhibitors as potent anticancer drugs.组蛋白 H2A 丝氨酸 12 磷酸化酶(Haspin):作为设计强效抗癌药物抑制剂的有前途的靶标。
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Increased MIR31HG lncRNA expression increases gefitinib resistance in non-small cell lung cancer cell lines through the EGFR/PI3K/AKT signaling pathway.MIR31HG长链非编码RNA表达增加通过EGFR/PI3K/AKT信号通路增强非小细胞肺癌细胞系对吉非替尼的耐药性。
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Haspin kinase regulates microtubule-organizing center clustering and stability through Aurora kinase C in mouse oocytes.在小鼠卵母细胞中,Haspin激酶通过极光激酶C调节微管组织中心的聚集和稳定性。
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Targeted Therapy and Immunotherapy for Lung Cancer.肺癌的靶向治疗与免疫治疗
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[Treatment of advanced non-small-cell lung cancer with driver mutations].[驱动基因突变型晚期非小细胞肺癌的治疗]
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敲低 GSG2 抑制非小细胞肺癌的发展和进展。

Knockdown of GSG2 inhibits the development and progression of non-small cell lung cancer and .

机构信息

Department of thoracic surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Department of central disease control, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

出版信息

Cell Cycle. 2023 Jan;22(2):153-164. doi: 10.1080/15384101.2022.2110441. Epub 2022 Aug 16.

DOI:10.1080/15384101.2022.2110441
PMID:35972887
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9817127/
Abstract

Lung cancer has been recognized as the most common malignant neoplasm of the respiratory system with extremely high morbidity, among which non-small cell lung cancer (NSCLC) accounts for the majority. Many published literatures have revealed the roles of GSG2 in the progression of ovarian cancer, bladder cancer and breast cancer. However, there were no reports on the relationship between GSG2 and NSCLC. Herein, GSG2 was identified as a potential tumor promoter in NSCLC development, whose abundant expression was observed in NSCLC tissues compared with adjacent nonmalignant tissues and statistically correlated with more advanced tumor stage, more malignant grade and higher risk of lymphatic metastasis. Subsequent loss-of-function experiments indicated that GSG2 depletion could arrest cell cycle and suppress cell proliferation and migration while enhancing cell apoptosis. At the same time, the suppressive effects of GSG2 depletion on NSCLC development were verified by experiments. In conclusion, the current study identified GSG2 as a tumor promoter in development and progression of NSCLC, which could work as a novel therapeutic target for NSCLC.

摘要

肺癌已被公认为呼吸系统最常见的恶性肿瘤,发病率极高,其中非小细胞肺癌(NSCLC)占大多数。许多已发表的文献揭示了 GSG2 在卵巢癌、膀胱癌和乳腺癌进展中的作用。然而,目前还没有关于 GSG2 与 NSCLC 之间关系的报道。本研究鉴定出 GSG2 是 NSCLC 发展中的一种潜在的肿瘤促进因子,与相邻的非恶性组织相比,GSG2 在 NSCLC 组织中大量表达,且与更晚期的肿瘤分期、更恶性的分级和更高的淋巴转移风险显著相关。随后的功能丧失实验表明,GSG2 耗竭可使细胞周期停滞,并抑制细胞增殖和迁移,同时增强细胞凋亡。同时,通过实验验证了 GSG2 耗竭对 NSCLC 发展的抑制作用。总之,本研究鉴定出 GSG2 是 NSCLC 发生和发展中的一种肿瘤促进因子,可作为 NSCLC 的一个新型治疗靶点。