Article
Pharmacology & Pharmacy
Dan Shen, Yuanyuan Zeng, Weijie Zhang, Yue Li, Jianjie Zhu, Zeyi Liu, Zhaowei Yan, Jian-An Huang
Summary: In this study, it was found that Chenodeoxycholic acid (CDCA) attenuates the pathogenesis of lung adenocarcinoma (LUAD) in vitro and in vivo via the integrin alpha 5131/FAK/p53 axis.
EUROPEAN JOURNAL OF PHARMACOLOGY
(2022)
Article
Oncology
Daniele Tavernari, Elena Battistello, Elie Dheilly, Aaron S. Petruzzella, Marco Mina, Jessica Sordet-Dessimoz, Solange Peters, Thorsten Krueger, David Gfeller, Nicolo Riggi, Elisa Oricchio, Igor Letovanec, Giovanni Ciriello
Summary: This study provides a detailed molecular map of intratumor spatial heterogeneity in lung adenocarcinoma, revealing non-genetic routes of cancer evolution. The transition from indolent to aggressive patterns in tumors is driven by epigenetic and transcriptional reprogramming reshaping cancer cell identity rather than genetic alterations. Highly multiplexed protein spatial profiling shows the coexistence of immune desert, inflamed, and excluded regions within individual tumors, matching histologic pattern composition.
Article
Biology
Hou-Fu Guo, Neus Bota-Rabassedas, Masahiko Terajima, B. Leticia Rodriguez, Don L. Gibbons, Yulong Chen, Priyam Banerjee, Chi-Lin Tsai, Xiaochao Tan, Xin Liu, Jiang Yu, Michal Tokmina-Roszyk, Roma Stawikowska, Gregg B. Fields, Mitchell D. Miller, Xiaoyan Wang, Juhoon Lee, Kevin N. Dalby, Chad J. Creighton, George N. Phillips, John A. Tainer, Mitsuo Yamauchi, Jonathan M. Kurie
Summary: Guo et al. have determined the molecular basis of collagen lysyl hydroxylase 2 (LH2) substrate specificity, showing that LH2 functions not only as a telopeptidyl lysyl hydroxylase, but also as a collagen glucosyltransferase to drive lung cancer progression. The research suggests that LH2 plays a crucial role in promoting LUAD progression through a variety of mechanisms, including tLH-dependent and tLH-independent pathways.
COMMUNICATIONS BIOLOGY
(2021)
Editorial Material
Oncology
Zahraa Rahal, Humam Kadara
Summary: Increasing evidence suggests that tumors have diverse microbiomes, which adds complexity to the tumor microenvironment. This study highlights the role of the intratumor mycobiome, specifically Aspergillus sydowii, in promoting lung adenocarcinoma progression through the IL-1b signaling pathway.
Article
Oncology
Hui-er Zhu, Tao Li, Shengnan Shi, De-xiong Chen, Weiping Chen, Hui Chen
Summary: The study demonstrates that ESCO2 promotes proliferation and metastasis of LUAD cells through metabolic reprogramming both in vitro and in vivo. Mechanistically, ESCO2 inhibits hnRNPA1 nuclear translocation, leading to increased binding of hnRNPA1 to the intronic sequences flanking exon 9 of PKM mRNA, ultimately inhibiting PKM1 isoform formation and inducing PKM2 isoform formation.
JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
(2021)
Article
Cell Biology
Xin Peng, Xiaoli Liu, Wanshan Hu, Yanling Zhou, Lianlian Ouyang, Xintong Peng, Yao Long, Jingyue Sun, Tania Tao, Ling Chen, Ying Shi, Yongguang Tao, Desheng Xiao, Shuang Liu
Summary: In lung adenocarcinoma, overexpression of HOXC11 is associated with worse survival and is regulated by IKK alpha. HOXC11 promotes lung cancer progression by enhancing the expression of SPHK1 through directly binding to its promoter region.
CELL DEATH & DISEASE
(2023)
Article
Biochemistry & Molecular Biology
Tao Fan, Shuofeng Li, Chu Xiao, He Tian, Yujia Zheng, Yu Liu, Chunxiang Li, Jie He
Summary: CCL20 plays a role in promoting lung adenocarcinoma progression, with high expression associated with poor prognosis and activation of EMT, inflammatory response, and TNF pathway. Knockdown of CCL20 inhibits EMT process and cell proliferation in lung adenocarcinoma. Low CCL20 expression improves response to anti-PD-L1 therapy.
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
(2022)
Article
Chemistry, Physical
Yayi He, Xiaogang Liu, Hao Wang, Liang Wu, Minlin Jiang, Haoyue Guo, Junjie Zhu, Shengyu Wu, Hui Sun, Shanhao Chen, Yuming Zhu, Caicun Zhou, Yang Yang
Summary: This study utilized single-cell RNA sequencing to analyze tumor and normal tissue from lung adenocarcinoma patients, providing insights into the heterogeneity and evolution of lung adenocarcinoma subtypes. The findings reveal changes in the immune microenvironment and development process of adenocarcinoma during lung cancer progression.
Article
Oncology
Qi Wen Chen, Qian Qian Cai, Ying Yang, Shu Dong, Yuan Yuan Liu, Zhong Yi Chen, Chun Lan Kang, Bing Qi, Yi Wei Dong, Wei Wu, Li Ping Zhuang, Ye Hua Shen, Zhi Qiang Meng, Xing Zhong Wu
Summary: This study reveals the important role and mechanism of long non-coding RNA BC in promoting tumor metastasis and influencing clinical prognosis of lung adenocarcinoma (LUAD). BC promotes growth, invasion, metastasis, and resistance to EGFR-targeted therapies in lung cancer by forming a splicing complex with nucleolin and hnRNPK. High expression of BC is associated with clinical progress and poor survival in LUAD.
CLINICAL AND TRANSLATIONAL MEDICINE
(2023)
Article
Oncology
Lecai Xiong, Yanhong Wei, Xiao Zhou, Peng Dai, Yi Cai, Xuefeng Zhou, Ming Xu, Jinping Zhao, Hexiao Tang
Summary: The AGTR1 gene is expressed less in most tumors but is associated with a better prognosis in lung adenocarcinoma. It is related to lymph node metastasis and MET mutation, as well as the anti-tumor immune microenvironment. Additionally, AGTR1 may play a role in LUAD through the PI3K/AKT3 pathway.
CANCER MANAGEMENT AND RESEARCH
(2021)
Article
Geriatrics & Gerontology
Xuan Wang, Zheng Wang, Renhong Huang, Zhouyi Lu, Xiaofeng Chen, Dayu Huang
Summary: UPP1 is identified as a novel oncogene in LUAD, playing a crucial role in LUAD cell progression. UPP1 drives glycolytic metabolism and is subject to epigenetic regulation through histone acetylation.
Article
Biochemical Research Methods
Ming Wang, Tianyu He, Di Meng, Wang Lv, Jiayue Ye, Ling Cheng, Jian Hu
Summary: This study found that BZW2 is highly expressed in LUAD tissues and is associated with poor prognosis. BZW2 promotes the malignant progression of LUAD by promoting lactate production and lactylation of IDH3G. Inhibition of Hla can suppress the malignant progression of LUAD.
JOURNAL OF PROTEOME RESEARCH
(2023)
Article
Biochemistry & Molecular Biology
Hua Zhong, Wen Lu, Yong Tang, Clotilde Wiel, Yong Wei, Jian Cao, Gregory Riedlinger, Thales Papagiannakopoulos, Jessie Yanxiang Guo, Martin O. Bergo, Yibin Kang, Shridar Ganesan, Hatim E. Sabaawy, Sharon R. Pine
Summary: The SOX9 transcription factor plays important roles in tissue development and homeostasis, and has been implicated in tumor progression. However, its role in lung adenocarcinoma (LUAD) is not well understood. In this study, researchers used genetic knockout approaches in a mouse model of LUAD and found that loss of Sox9 significantly reduces lung tumor development and progression. They also demonstrated that SOX9 suppresses immune cell infiltration and function, which contributes to the inhibition of anti-tumor immunity. These findings suggest that SOX9 drives lung tumor progression by modulating the tumor microenvironment.
Article
Medicine, General & Internal
Jun Shang, He Jiang, Yue Zhao, Jinglei Lai, Leming Shi, Jingcheng Yang, Haiquan Chen, Yuanting Zheng
Summary: Through whole-exome sequencing and RNA sequencing analysis of GGO-like lung adenocarcinoma, we identified differences compared to solid nodule lung adenocarcinoma, including lower TP53 mutation frequency and less active cell proliferation-related pathways. We also found differences between GGO-like lung adenocarcinoma and minimally invasive adenocarcinoma in terms of EGFR mutation frequency, CNV load, and immune cell abundance. Finally, we developed a transcriptomic signature that predicts the progression from GGO to solid nodule and patients' prognosis.
Article
Oncology
Suping Tang, Jun Ni, Bohua Chen, Fei Sun, Jinbo Huang, Songshi Ni, Zhiyuan Tang
Summary: Our study found that PAFAH1B3 is upregulated in LUAD tissues and cells compared with noncancerous tissues and cells. It is positively correlated with distant metastasis, TNM stage, and poor clinical outcome, and serves as an independent prognostic risk factor for LUAD. Silencing PAFAH1B3 suppresses proliferation, invasion, and EMT, while increasing the cell population in the G0-G1 phases. Additionally, knockdown of PAFAH1B3 increases E-cadherin level and decreases N-cadherin level, inhibiting tumorigenesis and neutrophil infiltration in the xenograft tumor model.