Article
Biotechnology & Applied Microbiology
Fangfang Gao, Xiaoqian Mu, Huijuan Wu, Lijuan Chen, Jie Liu, Yanqiu Zhao
Summary: Calreticulin (CALR) is aberrantly expressed in lung cancer, and its overexpression promotes proliferation of lung cancer cells, possibly through activation of the NF-kappa B signaling pathway.
Article
Biochemical Research Methods
Chance M. Nowak, Tyler Quarton, Leonidas Bleris
Summary: The study reveals that cells rapidly become asynchronous after synchronization, and the factors controlling this process are largely unknown. Through experiments and simulations, it is found that the variability in cell cycle duration is the main factor causing cell desynchronization, which provides new insights into cell cycle research.
PLOS COMPUTATIONAL BIOLOGY
(2023)
Article
Medicine, Research & Experimental
Xiao-jie Jiang, Zhi-wei Chen, Jian-feng Zhao, Chang-xi Liao, Qing-he Cai, Jing Lin
Summary: The study investigated the role of cIAP2 in hepatocellular carcinoma, finding that high cIAP2 expression was associated with poor prognosis. Knocking down cIAP2 reduced cell proliferation, invasion, and NF-kappa B pathway activity. Animal experiments showed that cIAP2 knockdown reduced tumourigenicity and proliferation activity in liver cancer cells.
Article
Genetics & Heredity
Huajie Mao, Ya Zhao, Li Lei, Yanxia Hu, Hangrui Zhu, Runzhi Wang, Dongsheng Ni, Jianing Liu, Lei Xu, Hua Xia, Zaikuan Zhang, Meng Ma, Zheng Pan, Qin Zhou, Yajun Xie
Summary: SELS is highly expressed in clear cell renal cell carcinoma (ccRCC) and associated with multiple pathological features. SELS overexpression promotes cell proliferation and inhibits apoptosis, while silence of SELS has the opposite effect. Mechanistically, SELS activates AKT/GSK3 beta/NF-kappa B signaling pathway to enhance cell proliferation and inhibit apoptosis, and stabilizes c-Myc by preventing ubiquitin-proteasome-mediated degradation. Furthermore, SELS inhibits ccRCC cell migration likely through repressing epithelial-mesenchymal transition (EMT).
Article
Biochemistry & Molecular Biology
Inho Kang, Ji Ae Kim, Jinchul Kim, Ju Hyeon Lee, Mi-Jee Kim, Jeong Keun Ahn
Summary: Hepatitis B virus (HBV) infection is a major cause of hepatocellular carcinoma (HCC). In this study, the researchers discovered a new mechanism of HBV-associated HCC metastasis. HBV X protein (HBx) interacts with the suppressor of cytokine signaling 1 (SOCS1), resulting in the activation of NF-kappa B and the transcription of factors associated with epithelial-mesenchymal transition (EMT), which promotes the invasiveness and migration of cancer cells.
Article
Gastroenterology & Hepatology
Suzanne Faure-Dupuy, Tobias Riedl, Maude Rolland, Zoheir Hizir, Florian Reisinger, Katharina Neuhaus, Svenja Schuehle, Caroline Remouchamps, Nicolas Gillet, Maximilian Schoenung, Mira Stadler, Jochen Wettengel, Romain Barnault, Romain Parent, Linda Christina Schuster, Rayan Farhat, Sandra Prokosch, Corinna Leuchtenberger, Rupert Oellinger, Thomas Engleitner, Karsten Rippe, Roland Rad, Kristian Unger, Darjus Tscharahganeh, Daniel B. Lipka, Ulrike Protzer, David Durantel, Julie Lucifora, Emmanuel Dejardin, Mathias Heikenwalder
Summary: The study identified the essential role of canonical and non-canonical NF-kappa B signaling pathways in A3B induction and anti-HBV effects, as well as the post-transcriptional regulation of A3B expression by miRNA 138-5p. Treatment with a LT beta R-specific agonist for 12 days significantly reduced the cccDNA pool without affecting cancer-related host genes, indicating the potential of A3B-mediated cccDNA decay as a therapeutic strategy against chronic HBV infection.
Article
Oncology
Ming Li, Yubo Xiao, Pinyue Liu, Le Wei, Ti Zhang, Ziye Xiang, Xiaoyan Liu, Keyun Zhang, Qiaoqing Zhong, Fangzhi Chen
Summary: 4-Methoxydalbergione (4-MD) is capable of inhibiting the progression of certain cancers, however, its effects on esophageal cancer (EC) were unclear. The present study aimed to investigate the inhibitory effect of 4-MD on EC and its molecular mechanism. Results showed that 4-MD treatment significantly inhibited proliferation and migration, downregulated inflammatory cytokines, and inactivated the NF-kappa B signaling pathway. Additionally, 4-MD reversed the increases induced by lipopolysaccharide (LPS) in EC cells. These findings suggest that 4-MD may attenuate EC cell proliferation and migration by inactivating the NF-kappa B signaling pathway.
Article
Oncology
Xiao Liu, Meng Jiang, Chenggang Pang, Jianning Wang, Lijuan Hu
Summary: In this study, sodium selenite (SSE) was found to inhibit proliferation and migration and induce apoptosis in renal cancer cells. The underlying mechanism involves the regulation of reactive oxygen species (ROS) levels and inhibition of NF-kappa B signaling. The inhibitory effect of SSE on tumor growth was also confirmed in animal models.
Article
Biochemistry & Molecular Biology
Sang Eun Ha, Seong Min Kim, Preethi Vetrivel, Hun Hwan Kim, Pritam Bhagwan Bhosale, Jeong Doo Heo, Ho Jeong Lee, Gon Sup Kim
Summary: SCU as a potential agent for HCC therapy inhibits cell proliferation and metastasis in HepG2 cells through upregulation of PTEN and inhibition of the PI3K/Akt/NF-kappa B signaling pathway. It is a natural based agent that shows promise in improving therapeutic outcomes for HCC treatment.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Biochemistry & Molecular Biology
Jiayao Qu, Jia Li, Yaming Zhang, Rongzhang He, Xiangting Liu, Ke Gong, Lili Duan, Weihao Luo, Zheng Hu, Gengsheng Wang, Chenglai Xia, Dixian Luo
Summary: Elevated expression of AKR1B10 in breast cancer tissues was associated with lymph node metastasis, tumor size, Ki67 expression, and p53 expression, while inversely correlated with overall and disease-free survival rates. AKR1B10 promotes proliferation, migration, and invasion of breast cancer cells via the PI3K/AKT/NF-kappa B signaling pathway, indicating its potential as a prognostic indicator and therapeutic target in breast cancer.
CELL AND BIOSCIENCE
(2021)
Article
Oncology
Yen-Yun Wang, Amos C. Hung, Steven Lo, Shyng-Shiou F. Yuan
Summary: Obesity is a major modifiable risk factor for breast cancer, with adipocytokines like visfatin and resistin playing important roles in tumor-stromal interactions and breast cancer development. Therapeutic strategies targeting these adipocytokines hold promise for novel breast cancer therapies.
Article
Multidisciplinary Sciences
Bingling Dai, Hanbing Cao, Yu Hu, Zhengyan Gong, Xiaoyue Huang, Yanbin Chen, Feng Liu, Xiujuan Peng, Yanmin Zhang, Xinjun Lei
Summary: This study observed low expression levels of the NLRP3 inflammasome in a subset of HCC cells and demonstrated the activation of NLRP3 inflammasome through the nuclear factor kappa B signaling pathway by LPS + ATP. The activation of NLRP3 inflammasome inhibited HCC cell proliferation, arrested the cell cycle at the G1 phase, and suppressed cell migration.
Review
Immunology
Xinyu Lu, Qianhui Chen, Hongyan Liu, Xiaoyong Zhang
Summary: The non-canonical NF-kappa B signaling pathway is crucial in HBV infection, influencing host immune responses, viral replication, and liver damage. Understanding the interaction between HBV and this pathway may lead to the discovery of potential therapeutic targets and drugs for treating HBV infection.
FRONTIERS IN IMMUNOLOGY
(2021)
Article
Orthopedics
Yunshan Guo, Jinzhu Fan, Shuguang Liu, Dingjun Hao
Summary: This study reveals that downregulation of Orai1 may reduce cyclin D1 expression by inactivating the Ras-NF-kappa B signaling pathway, thus blocking osteoblast proliferation and cell cycle.
BMC MUSCULOSKELETAL DISORDERS
(2022)
Article
Biochemistry & Molecular Biology
Lei Xu, Yangfan Ye, Zeqiang Tao, Tian Wang, Yutian Wei, Wanzhi Cai, Xin Wan, Pengzhan Zhao, Wei Gu, Bin Gu, Liuchao Zhang, Yufei Tian, Ning Liu, Yiming Tu, Jing Ji
Summary: This study elucidated the role of MLPH in GBM radiation resistance, showing that MLPH promotes radiotherapy resistance by regulating the NF-kappa B pathway. Additionally, O-GlcNAcylation of MLPH protects it from degradation and stabilizes its presence in cells. These findings provide insights into a potential mechanism of GBM radiation resistance and suggest a therapeutic strategy for GBM treatment.
