Article
Immunology
Allison P. Drain, Nastaran Zahir, Jason J. Northey, Hui Zhang, Po-Jui Huang, Ori Maller, Johnathon N. Lakins, Xinmiao Yu, Jennifer L. Leight, Brenda P. Alston-Mills, E. Shelley Hwang, Yunn-Yi Chen, Catherine C. Park, Valerie M. Weaver
Summary: Triple-negative breast cancers are associated with poor survival due to treatment resistance. The stiffness of the extracellular matrix (ECM) affects treatment response, with soft ECM promoting treatment resistance and stiff ECM sensitizing cells to treatment. Agents that modulate stiffness-dependent NF-kappa B or JNK activity could enhance therapeutic efficacy in patients with TNBC.
JOURNAL OF EXPERIMENTAL MEDICINE
(2021)
Article
Immunology
Allison P. Drain, Nastaran Zahir, Jason J. Northey, Hui Zhang, Po-Jui Huang, Ori Maller, Johnathon N. Lakins, Xinmiao Yu, Jennifer L. Leight, Brenda P. Alston-Mills, E. Shelley Hwang, Yunn-Yi Chen, Catherine C. Park, Valerie M. Weaver
Summary: Soft extracellular matrix protects breast cancer cells from apoptosis, reduces the efficacy of chemo- and radiation therapies, and enhances NF-kappa B signaling while diminishing proapoptotic JNK activity. Therapeutic targeting of the NF-kappa B-JNK axis may help overcome treatment resistance in breast cancer, particularly in triple-negative breast cancers (TNBCs). Residual TNBCs residing in a softer stromal microenvironment exhibit elevated NF-kappa B activity and compromised JNK activity, contributing to treatment resistance.
JOURNAL OF EXPERIMENTAL MEDICINE
(2021)
Article
Oncology
Shu Liu, Yewei Zhang, Shien Cui, Dajiang Song, Bo Li, Qian Chen, Guangyu Yao, Bin Gong
Summary: This study reveals the upregulation of NAP1L1 in breast cancer and its interaction with HDGF to recruit c-Jun, leading to cell growth. NAP1L1 may serve as a potential oncogene with therapeutic implications for breast cancer treatment.
CANCER CELL INTERNATIONAL
(2021)
Article
Oncology
Ping Zhu, Guoping Liu, Xue Wang, Jingjing Lu, Yue Zhou, Shuyi Chen, Yabiao Gao, Chaofu Wang, Jerry Yu, Yangbai Sun, Ping Zhou
Summary: The study revealed that GLUT1 mRNA expression is significantly increased in breast cancer tissues, which is associated with metastasis and poor prognosis. The transcription factor c-Jun may regulate GLUT1 gene expression by binding to its promoter, thereby affecting glycolysis and breast cancer metastasis.
Article
Chemistry, Multidisciplinary
Cong-hui Zhang, Hong Liu, Wu-li Zhao, Wen-xia Zhao, Hui-min Zhou, Rong-guang Shao
Summary: The study revealed that G3BP1 is upregulated and correlated with poor prognosis in breast cancer. Overexpression of G3BP1 promotes breast cancer cell proliferation by stimulating beta-catenin signaling. G3BP1 interacts with GSK-3 beta to inhibit beta-catenin degradation, thus enhancing the proliferative capacity of breast cancer cells.
ACTA PHARMACOLOGICA SINICA
(2021)
Review
Oncology
Alberto M. Martelli, Camilla Evangelisti, Francesca Paganelli, Francesca Chiarini, James A. McCubrey
Summary: GSK-3 consists of two isoforms, alpha and beta, that are constitutively active but can be inactivated through phosphorylation by upstream kinases. It was initially considered a tumor suppressor, but it has also been found to have oncogenic properties in promoting pathways critical for cancer cell proliferation, survival, and drug-resistance.
Article
Biochemistry & Molecular Biology
Hsuan-Yeh Pan, Mallika Valapala
Summary: Autophagy is a vital cellular mechanism that ensures cellular maintenance and survival. The GSK-3 signaling pathway regulates autophagy by modulating TFEB and other signaling molecules.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Cell Biology
Wenlong Hu, Jie Shen, Yu Tao, Dan Donga, Sicheng Lu, Liu Li, Dongdong Sun, Minmin Fan, Changliang Xu, Weixing Shen, Chengtao Yu, Haibo Cheng
Summary: This study found that CCDC85C inhibits the proliferation and migration of colorectal cancer cells by binding to GSK-3 beta and promoting ubiquitination and degradation of beta-catenin.
CELLULAR SIGNALLING
(2023)
Article
Biochemistry & Molecular Biology
Shihab Kochumon, Amnah Al-Sayyar, Texy Jacob, Amal Hasan, Fahd Al-Mulla, Sardar Sindhu, Rasheed Ahmad
Summary: TNF-α induces IP-10 expression in MCF-7 breast cancer cells through activation of the JNK/c-Jun signaling pathway.
Review
Pharmacology & Pharmacy
Noelia Miret, Carolina A. Pontillo, Sol Bujan, Florencia A. Chiappini, Andrea S. Randi
Summary: This literature review addresses the role of the aryl hydrocarbon receptor (AhR) and its ligands in breast cancer. The study explores the biological mechanisms of AhR agonists in interfering with breast endocrine functions and their impact on breast cancer development and progression. The findings suggest that exposure to AhR agonists stimulates pathways that promote breast cancer and contribute to tumor progression. Therefore, the evaluation and regulation of industrial and agricultural chemicals and other toxicants are essential in reducing the risk of breast cancer.
BIOCHEMICAL PHARMACOLOGY
(2023)
Review
Biochemistry & Molecular Biology
Licen Li, Chu-Xia Deng, Qiang Chen
Summary: SRC-3, also known as AIB1, is a member of the SRC family and plays a crucial role in regulating the transcriptional activity of nuclear receptors and promoting cancer development. Understanding the mode of action of SRC-3 can provide insights for cancer therapy.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Biochemistry & Molecular Biology
Thu H. Truong, Elizabeth A. Benner, Kyla M. Hagen, Nuri A. Temiz, Carlos Perez Kerkvliet, Ying Wang, Emilio Cortes-Sanchez, Chieh-Hsiang Yang, Thomas Pengo, Katrin P. Guillen, Bryan E. Welm, Sucheta Telang, Carol A. Lange, Julie H. Ostrander, Marygrace C. Trousdell, Camila
Summary: Recurrence of metastatic breast cancer in women with luminal (ER+) breast cancer is a significant health burden, with contributing factors including the maintenance and expansion of breast cancer stem cells. The study demonstrates that cytoplasmic complexes composed of steroid receptor co-activators PELP1 and SRC-3 modulate breast cancer stem cell expansion by upregulating metabolic target genes PFKFB3 and PFKFB4. This suggests a potential new approach to overcoming endocrine and chemotherapy resistance in ER+ tumor cell populations.
Article
Biochemistry & Molecular Biology
Seng Chuan Tang, Quentin Lion, Olivier Peulen, Philippe Chariot, Arnaud Lavergne, Alice Mayer, Paula Allepuz Fuster, Pierre Close, Sebastian Klein, Alexandra Florin, Reinhard Buettner, Ivan Nemazanyy, Kateryna Shostak, Alain Chariot
Summary: COP1 acts as an oncogenic E3 ligase by promoting ERα signaling but also acts as a tumor suppressor candidate by preventing EMT, reflecting a dual role of COP1 in breast cancer that has sparked widespread interest in the academic community.
Article
Biotechnology & Applied Microbiology
Ming Lei, Kangcheng Zhao, Wenbin Hua, Kun Wang, Shuai Li, Xinghuo Wu, Cao Yang
Summary: The study demonstrated that overexpression of c-Jun has a positive effect on the treatment of intervertebral disc degeneration, inhibiting the inflammatory response in vivo and potentially delaying the degeneration of the intervertebral disc.
Article
Medicine, Research & Experimental
Qian Li, Xuejiao Lv, Chunyong Han, Yu Kong, Zhongye Dai, Dawei Huo, Ting Li, Dapeng Li, Wei Li, Xing Wang, Qian Zhao, Jie Ming, Wen Yang, Yang Chen, Xudong Wu
Summary: This study investigates the transcriptomic and epigenomic features of NFs and CAFs associated with breast cancer metastasis, and identifies signature genes and enhancers specific to CAFs. The study demonstrates the importance of activated JUN in remodeling enhancers and maintaining the activation of CAF-specific enhancers, leading to breast cancer invasiveness. These findings provide insights into stroma cell transformation and support the potential of stroma-targeting strategy in cancer treatment.
Correction
Oncology
Valerie M. Jansen, Neil E. Bhola, Joshua A. Bauer, Luigi Formisano, Kyung-Min Lee, Katherine E. Hutchinson, Agnieszka K. Witkiewicz, Preston D. Moore, Onica Valeria Estrada, Violeta Sanchez, Paula G. Ericsson, Melinda E. Sanders, Paula R. Pohlmann, Michael J. Pishvaian, David A. Riddle, Teresa C. Dugger, Wenyi Wei, Erik S. Knudsen, Carlos L. Arteaga
Correction
Oncology
Sarah Croessmann, Jonathan H. Sheehan, Kyung-min Lee, Gregory Sliwoski, Jie He, Rebecca Nagy, David Riddle, Ingrid A. Mayer, Justin M. Balko, Richard Lanman, Vincent A. Miller, Lewis C. Cantley, Jens Meiler, Carlos L. Arteaga
CLINICAL CANCER RESEARCH
(2019)
Correction
Oncology
Dhivya R. Sudhan, Angel Guerrero-Zotano, Helen Won, Paula Gonzalez Ericsson, Alberto Servetto, Mariela Huerta-Rosario, Dan Ye, Kyung-min Lee, Luigi Formisano, Yan Guo, Qi Liu, Lisa N. Kinch, Monica Red Brewer, Teresa Dugger, James Koch, Michael J. Wick, Richard E. Cutler, Alshad S. Lalani, Richard Bryce, Alan Auerbach, Ariella B. Hanker, Carlos L. Arteaga
Article
Oncology
Dhivya R. Sudhan, Angel Guerrero-Zotano, Helen Won, Paula Gonzalez Ericsson, Alberto Servetto, Mariela Huerta-Rosario, Dan Ye, Kyung-min Lee, Luigi Formisano, Yan Guo, Qi Liu, Lisa N. Kinch, Monica Red Brewer, Teresa Dugger, James Koch, Michael J. Wick, Richard E. Cutler, Alshad S. Lalani, Richard Bryce, Alan Auerbach, Ariella B. Hanker, Carlos L. Arteaga
Article
Oncology
Alberto Servetto, Rahul Kollipara, Luigi Formisano, Chang-Ching Lin, Kyung-Min Lee, Dhivya R. Sudhan, Paula I. Gonzalez-Ericsson, Sumanta Chatterjee, Angel Guerrero-Zotano, Saurabh Mendiratta, Hiroaki Akamatsu, Nicholas James, Roberto Bianco, Ariella B. Hanker, Ralf Kittler, Carlos L. Arteaga
Summary: FGFR1 overexpression in the nucleus of breast cancer cells is associated with endocrine resistance in ER+ breast cancer. Nuclear FGFR1 influences gene transcription and promotes resistance to estrogen suppression and fulvestrant. Treatment with FGFR tyrosine kinase inhibitors does not affect nuclear FGFR1 activity, supporting the development of strategies to inhibit nuclear FGFR1 in ER+/FGFR1 overexpressing breast cancer.
CLINICAL CANCER RESEARCH
(2021)
Article
Oncology
Ariella B. Hanker, Benjamin P. Brown, Jens Meiler, Arnaldo Marin, Harikrishna S. Jayanthan, Dan Ye, Chang-Ching Lin, Hiroaki Akamatsu, Kyung-Min Lee, Sumanta Chatterjee, Dhivya R. Sudhan, Alberto Servetto, Monica Red Brewer, James P. Koch, Jonathan H. Sheehan, Jie He, Alshad S. Lalani, Carlos L. Arteaga
Summary: The study found that the frequent HER3(E928G) kinase domain mutation increases the affinity of HER2/HER3 and reduces the binding of HER2 to its inhibitor neratinib. Co-expression of mutant HER2/HER3 enhances HER2/HER3 co-immunoprecipitation and ligand-independent activation of HER2/HER3 and PI3K/AKT, leading to increased growth, invasiveness, and resistance to HER2-targeted therapies, which can be reversed by combined treatment with PI3K alpha inhibitors.
Article
Oncology
Kyung-min Lee, Chang-Ching Lin, Alberto Servetto, Joonbeom Bae, Vishal Kandagatla, Dan Ye, GunMin Kim, Dhivya R. Sudhan, Saurabh Mendiratta, Paula I. Gonzalez Ericsson, Justin M. Balko, Jeon Lee, Spencer Barnes, Venkat S. Malladi, Siamak Tabrizi, Sangeetha M. Reddy, Seoyun Yum, Ching-Wei Chang, Katherine E. Hutchinson, Susan E. Yost, Yuan Yuan, Zhijian J. Chen, Yang-Xin Fu, Ariella B. Hanker, Carlos L. Arteaga
Summary: MYC suppression in TNBC leads to immune-related gene expression and tumor-infiltrating T cells. Mechanistically, MYC represses STING expression, resulting in downregulation of T-cell chemokines. Inhibiting MYC and using PD-L1 blockade can restore sensitivity to PD-L1 inhibitors in MYC-overexpressing TNBC.
CANCER IMMUNOLOGY RESEARCH
(2022)
Review
Biochemistry & Molecular Biology
Hyungjoo Kim, Je-Min Choi, Kyung-min Lee
Summary: Immune checkpoint blockades have greatly improved cancer treatment, but a significant number of TNBC patients do not respond to these therapies, and mechanisms of resistance are poorly understood. This review focuses on biomarkers and recent advances in understanding molecular mechanisms of resistance to ICBs in TNBC.
Article
Cell Biology
Tae Won Lee, Kyung-min Lee
Summary: ECM1 plays a role in promoting endocrine resistance in ER+ breast cancers, and its high expression is associated with poor response to endocrine therapies in breast cancer patients.
ANIMAL CELLS AND SYSTEMS
(2022)
Article
Multidisciplinary Sciences
Kyung-min Lee, Angel L. Guerrero-Zotano, Alberto Servetto, Dhivya R. Sudhan, Chang-Ching Lin, Luigi Formisano, Valerie M. Jansen, Paula Gonzalez-Ericsson, Melinda E. Sanders, Thomas P. Stricker, Ganesh Raj, Kevin M. Dean, Reto Fiolka, Lewis C. Cantley, Ariella B. Hanker, Carlos L. Arteaga
NATURE COMMUNICATIONS
(2020)
Meeting Abstract
Oncology
Kyung-min Lee, Angel Guerrero-Zotano, Ariella Hanker, Alberto Servetto, Dhivya Sudhan, Luigi Formisano, Valerie Jansen, Paula Gonzalez-Ericsson, Melinda Sanders, Thomas Stricker, Lewis Cantley, Carlos Arteaga
Meeting Abstract
Oncology
Alberto Servetto, Rahul Kollipara, Luigi Formisano, Kyung-min Lee, Dhivya R. Sudhan, Ariella B. Hanker, Sumanta Chatterjee, Albert Lin, Saurabh Mendiratta, Nicholas James, Ralf Kittler, Carlos L. Arteaga
Article
Oncology
Hitisha K. Patel, Nianjun Tao, Kyung-Min Lee, Mariela Huerta, Heike Arlt, Tara Mullarkey, Steven Troy, Carlos L. Arteaga, Teeru Bihani
BREAST CANCER RESEARCH
(2019)
Meeting Abstract
Oncology
Alberto Servetto, Luigi Formisano, Rahul Kollipara, Dhivya R. Sudhan, Kyung-min Lee, Sumanta Chatterjee, Ariella B. Hanker, Saurabh Mendiratta, Ralf Kittler, Carlos L. Arteaga
Correction
Oncology
Kyung-min Lee, Keesoo Nam, Sunhwa Oh, Juyeon Lim, Young-Pil Kim, Jong Won Lee, Jong-Han Yu, Sei-Hyun Ahn, Sung-Bae Kim, Dong-Young Noh, Taehoon Lee, Incheol Shin
BREAST CANCER RESEARCH
(2019)
Article
Cell Biology
Ke Mi, Lizhong Zeng, Yang Chen, Jingya Ning, Siyuan Zhang, Peilin Zhao, Shuanying Yang
Summary: In this study, the researchers explored the role of DHX38 in NSCLC and its underlying molecular mechanism. They found that DHX38 was overexpressed in NSCLC and patients with high DHX38 expression had poor prognosis. DHX38 promoted cell proliferation, migration, and invasion in NSCLC and activated the MAPK pathway. The researchers also identified G3BP1 as a target protein that interacted with DHX38 and showed that DHX38 regulated the expression of G3BP1. Silencing G3BP1 reversed the effects of DHX38 overexpression on tumor cell proliferation, migration, and invasion and inhibited the MAPK pathway activation.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Tiina A. Jokela, Mark A. Dane, Rebecca L. Smith, Kaylyn L. Devlin, Sundus Shalabi, Jennifer C. Lopez, Masaru Miyano, Martha R. Stampfer, James E. Korkola, Joe W. Gray, Laura M. Heiser, Mark A. Labarge
Summary: Microenvironment signals have a significant impact on cell fate and tissue homeostasis. Understanding how different microenvironment factors regulate cellular phenotype has been challenging. In this study, a high-throughput microenvironment microarray was used to identify factors that support the proliferation and maintenance of primary human mammary luminal epithelial cells. Multiple factors that modulate luminal cell number were identified and their effects were confirmed using RNA sequencing and cell-based functional studies. Hepatocyte growth factor (HGF) was found to be robust to individual variation and played a role in expanding luminal cells. Our approach demonstrates the power of high-dimensional cell-based approaches in dissecting microenvironmental signals.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Chao He, Yongfeng Ding, Yan Yang, Gang Che, Fei Teng, Haohao Wang, Jing Zhang, Donghui Zhou, Yanyan Chen, Zhan Zhou, Haiyong Wang, Lisong Teng
Summary: This study categorized gastric cancer patients into three stemness subtypes, each demonstrating distinct prognoses, components of tumor microenvironment (TME) infiltration, and varying sensitivity or resistance to treatment. A stemness risk model was constructed to predict treatment response and prognosis.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Haile Zhao, Lijuan Feng, Rui Cheng, Man Wu, Xiaozhou Bai, Lifei Fan, Yaping Liu
Summary: miR-29c-3p is overexpressed in benign and malignant ovarian carcinoma and is associated with poor prognosis. Its overexpression modulates tumorigenesis in ovarian cancer cells, including epithelial-mesenchymal transition, proliferation, migration, and invasion, through the regulation of DNMT3A, TET1, and HBP1. miR-29c-3p may serve as a potential biomarker for clinical diagnosis or co-diagnosis of ovarian carcinoma.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Haiyan Zhao, Fangfang Bi, Mengyuan Li, Yuhan Diao, Chen Zhang
Summary: This study confirmed the tumor suppressor effect of RNF180 on ovarian cancer, elucidated the mechanism of the molecule network related to RNF180 and IPO4 in ovarian cancer, and identified a new therapeutic target for ovarian cancer.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Chu Chen, Guanhua Xu, Jiajia Chen, Chunshuai Wu, Jinlong Zhang, Jiawei Jiang, Hongxiang Hong, Zhiming Cui
Summary: This study investigated the role of transcription factor FoxO1 in facet joint osteoarthritis (FJOA) and found that FoxO1 deletion led to severe osteoarthritic changes. Transcriptome sequencing and bioinformatics analysis identified differentially expressed genes (DEGs) and potential key contributors to FJOA. Additionally, over-expression of certain genes and inhibition of others were shown to counteract the impairments caused by FoxO1 deletion in chondrocyte migration and extracellular matrix synthesis. These findings help unravel the molecular mechanisms underlying FJOA and open up promising therapeutic avenues for its treatment.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Wen Deng, Ru Chen, Situ Xiong, Jianqiang Nie, Hailang Yang, Ming Jiang, Bing Hu, Xiaoqiang Liu, Bin Fu
Summary: This study demonstrates that circFSCN1 is upregulated in bladder cancer and associated with cancer-specific survival. CircFSCN1 promotes tumor progression and epithelial-mesenchymal transition in bladder cancer through enhancing MDM2-mediated silencing of p53 by sponging miR-145-5p.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Jun Wu, Weibin Hu, Wenhui Yang, Yihao Long, Kaizhao Chen, Fugui Li, Xiaodong Ma, Xun Li
Summary: Cholesterol biosynthesis and metabolism play critical roles in tumor development and microenvironmental conditions. Squalene Epoxidase (SQLE), the second rate-limiting enzyme in cholesterol synthesis, is found to be uniquely expressed in various cancers, and its expression level is closely associated with tumor mutation burden and microsatellite instability. SQLE expression is negatively correlated with immune cell infiltration. Inhibition of SQLE alters the immune response in the tumor microenvironment. Furthermore, protein metabolism and translation are identified as main binding factors with SQLE.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Zhihong Zhang, Mingyue Li, Yi Tai, Yue Xing, Hongxiang Zuo, Xuejun Jin, Juan Ma
Summary: ZNF70 plays an important role in colitis-associated colorectal cancer (CAC) by regulating macrophages IL-1 beta secretion to promote HCT116 proliferation. It may serve as a promising target for treating CAC.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Zenghong Wu, Gangping Li, Weijun Wang, Kun Zhang, Mengke Fan, Yu Jin, Rong Lin
Summary: This study comprehensively explored the role of immune checkpoints and tumor microenvironment in gastric cancer patients based on genomic data. It constructed an ICIs signature and ICI score to evaluate patient prognosis and heterogeneity.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Yantong Wan, Jieshu Zhou, Panpan Zhang, Xuemei Lin, Hao Li
Summary: This study found that Rac1 plays a role in astrocyte activation and attenuates chronic inflammatory pain by blocking the phosphorylation of NLRP3 inflammasome and NF-kappa B.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Zhen Wang, Diankun She, Lei Liu, Xianming Hua, Hao Zhu, Lingfeng Yu, Han Wang, Yan Zhu, Gentao Fan, Yicun Wang, Meng Xu, Guangxin Zhou
Summary: Circular RNAs (circRNAs) are non-coding RNAs that play a role in the regulation of various cancers, including osteosarcoma (OS). This study identified circSATB2 as a highly expressed circRNA in OS tissues and cell lines, and demonstrated its involvement in promoting OS proliferation and migration. Mechanistically, circSATB2 was found to regulate the progression of OS by sponging miR-661 and FUS to regulate ZNFX1 mRNA. These findings suggest that circSATB2 could serve as a prognostic marker and therapeutic target for osteosarcoma.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Kenichi Ogata, Masafumi Moriyama, Tatsuya Kawado, Hiroki Yoshioka, Aiko Yano, Mayu Matsumura-Kawashima, Seiji Nakamura, Shintaro Kawano
Summary: This study found that extracellular vesicles released by induced pluripotent stem cells can reduce inflammatory cell infiltration, increase saliva volume, and decrease the production of antibodies associated with Sjogren's syndrome in a mouse model. The let-7 family in these vesicles may suppress the expression of TLR4 and NF-kappa B, which leads to the inhibition of pro-inflammatory cytokine production through the MAPK pathway.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Mikayla R. Erdelsky, Sarah A. Groves, Charmi Shah, Samantha B. Delios, M. Bibiana Umana, Donald H. Maurice
Summary: Recent evidence suggests that cAMP signaling within the primary cilium plays a crucial role in promoting adipogenic differentiation of 3T3-L1 preadipocytes. In this study, the researchers identified the specific cAMP phosphodiesterases expressed by these cells and found that inhibition of PDE4 promotes FFAR4-mediated adipogenesis. This work could potentially lead to the discovery of more targeted therapeutic approaches for controlling adipogenesis and differentiation of other stem cells.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Chun-Hui Liu, Jun-Jie Zhang, Qian-Jin Zhang, Yang Dong, Zhen-Duo Shi, Si-Hao Hong, Hou-Guang He, Wei Wu, Cong-Hui Han, Lin Hao
Summary: Bladder cancer, the most common malignant tumor in the urinary system, is associated with significantly up-regulated expression of P3H4, which is regulated by METTL3 and plays a crucial role in the proliferation, metastasis, and EMT progression of bladder cancer. Targeting this METTL3-P3H4 pathway may serve as a potential therapeutic strategy for bladder cancer.
CELLULAR SIGNALLING
(2024)