المؤلفون: Guanghui Wang, Yinghui Hu, Min Xu, Lihong Chen, Wenting Zhong

المصدر: Experimental Cell Research. 399:112448

مصطلحات موضوعية: 0301 basic medicine, Mice, Nude, Adenocarcinoma, Biology, DEAD-box RNA Helicases, Mice, 03 medical and health sciences, 0302 clinical medicine, Cell Movement, Stomach Neoplasms, Cell Line, Tumor, medicine, Animals, Humans, Neoplasm Invasiveness, RNA, Small Interfering, Protein kinase B, beta Catenin, Cell Proliferation, Gene knockdown, Glycogen Synthase Kinase 3 beta, Oncogene, Cell growth, Cancer, Cell Biology, Ribonucleoprotein, U2 Small Nuclear, medicine.disease, Gene Expression Regulation, Neoplastic, 030104 developmental biology, Gene Knockdown Techniques, 030220 oncology & carcinogenesis, Catenin, Cancer cell, Cancer research, Female, Signal transduction, Proto-Oncogene Proteins c-akt, Signal Transduction

الوصف: DEAD-box RNA helicase 46 (DDX46) has recently been identified as a candidate oncogene in several types of human malignancies. To date, the role of DDX46 in gastric cancer has not been determined. The purpose of the current study was to explore the role of DDX46 in gastric cancer and the potential mechanism. DDX46-silecing or overexpressing gastric cancer cell lines were established to validate the role of DDX46. Our results showed that the expression of DDX46 was significantly increased in gastric cancer tissues and cell lines. Knockdown of DDX46 suppressed the proliferation and invasion of gastric cancer cells. Whereas, DDX46 overexpression enhanced the cell proliferation and invasion of gastric cancer cells. Furthermore, knockdown of DDX46 markedly suppressed the tumor growth of xenografts. Research into the mechanism revealed that DDX46 depletion inhibited the Akt/GSK-3β/β-catenin signaling pathway in gastric cancer cells. Notably, activation of Akt or β-catenin overexpression reversed the DDX46 depletion-mediated anti-cancer effect. In conclusion, these findings indicated that DDX46 exerted an oncogenic role in gastric cancer via regulating the Akt/GSK-3β/β-catenin signaling pathway. Thus, DDX46 might be utilized as a therapeutic anti-cancer target.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e4be1aeea670c9a8aebbf6412cd38b4fTest
https://doi.org/10.1016/j.yexcr.2020.112448Test

المؤلفون: Tingyu Wu, Ximao Cui, Peng Du, Guanghui Wang, Chen-Ying Liu, Yun Liu, Tong Yu, Jinglue Song, Long Cui, Wenbin Shen, Yilian Zhu

المصدر: Journal of Cancer Research and Clinical Oncology. 143:971-980

مصطلحات موضوعية: Adult, Male, 0301 basic medicine, Cancer Research, Phosphorylase Kinase, Colorectal cancer, Mice, Nude, Biology, Gene Expression Regulation, Enzymologic, Metastasis, Mice, 03 medical and health sciences, 0302 clinical medicine, Biomarkers, Tumor, Tumor Cells, Cultured, medicine, Animals, Humans, Phosphorylase kinase, neoplasms, Aged, Cell Proliferation, Aged, 80 and over, Tissue microarray, Cell growth, General Medicine, Middle Aged, Cell cycle, HCT116 Cells, Prognosis, medicine.disease, digestive system diseases, Gene Expression Regulation, Neoplastic, 030104 developmental biology, Real-time polymerase chain reaction, Oncology, 030220 oncology & carcinogenesis, Cancer research, Immunohistochemistry, Female, Colorectal Neoplasms

الوصف: To study the expression and intracellular localization of phosphorylase kinase β (PHKβ) protein in colorectal cancers (CRCs), analyze its correlation with clinicopathological features and prognosis, and study the biological roles and mechanism-of-action of PHKβ in CRC cell lines. Quantitative polymerase chain reaction (qPCR) and western blot assays were performed to compare the expressions of PHKβ mRNA and protein in CRC tissues and matched normal mucosa. Tissue microarrays and immunohistochemical staining were performed to detect the expression and intracellular location of PHKβ protein and analyze its correlation with the clinicopathological characteristics and prognosis in CRC patients. Proliferation, cell cycle, wound healing, and xenograft models were used to elucidate the potential role of PHKβ in vitro and in vivo. PHKβ mRNA and protein were found to be overexpressed in CRC tissue compared to the levels in normal mucosa. Positive expression of PHKβ was significantly correlated with TNM stage and distal metastasis, and elevated expression of PHKβ was an independent prognostic factor in patients with CRC. PHKβ knockdown impaired proliferation of CRC in vitro and in vivo and induced cell cycle arrest. PHKβ affects CRC cell growth and represents a novel prognostic biomarker.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0b4936aeaac614acc4fc52069b0f064aTest
https://doi.org/10.1007/s00432-017-2362-1Test

المؤلفون: Yu Wu, Ting Lin, Zu-Jian Liao, Shuo Gao, Pei-Hsin Lin, Xiang-Zhong Liu, Mi Zhou, De-Quan Zeng, Wen-Jing Tian, Guanghui Wang, Jir-Mehng Lo, Daren Qiu, Hai-Feng Chen

المصدر: Chinese journal of natural medicines. 17(1)

مصطلحات موضوعية: Male, Alcoholic liver disease, Cholesterol, VLDL, Alcohol, 01 natural sciences, Terpene, 03 medical and health sciences, chemistry.chemical_compound, Mice, 0302 clinical medicine, Malondialdehyde, Drug Discovery, medicine, Animals, Aspartate Aminotransferases, Fruiting Bodies, Fungal, Antrodia, Liver Diseases, Alcoholic, Triglycerides, Liver injury, Biological Products, Traditional medicine, Triglyceride, biology, Ethanol, Molecular Structure, 010405 organic chemistry, Cholestenes, Alanine Transaminase, General Medicine, Aldehyde Dehydrogenase, medicine.disease, biology.organism_classification, Acute toxicity, Triterpenes, 0104 chemical sciences, Disease Models, Animal, Complementary and alternative medicine, chemistry, Liver, 030220 oncology & carcinogenesis, Female, Chemical and Drug Induced Liver Injury

الوصف: Antrodia camphorata, a well-known and highly valued edible medicinal mushroom with intriguing activities like liver protection, has been traditionally used for the treatment of alcoholic liver disease. A. camphorata shows highly medicinal and commercial values with the demand far exceeds the available supply. Thus, the petri-dish cultured A. camphorata (PDCA) is expected to develope as a substitute. In this paper, nineteen triterpenes were isolated from PDCA, and thirteen of them were the unique anthroic acids in A. camphorata, including the main content antcin K, which suggested that PDCA produced a large array of the same anthroic acids as the wild one. Furthermore, no obvious acute toxicity was found suggesting the edible safety of PDCA. In mice alcohol-induced liver injury model, triglyceride (TG), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA) had been reduced by the PDCA powder as well as the main content antcin K, which indicated that the PDCA could protect alcoholic liver injury in mice model and antcin K could be the effective component responsible for the hepatoprotective activities of PDCA against alcoholic liver diseases.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fb7ec0eed4ca3f5722e5a0812ad1ae0aTest
https://pubmed.ncbi.nlm.nih.gov/30704622Test

المؤلفون: Guanghui Wang, Xuqi Li, Cancan Zhou, Xinming Chang, Guanglin Qiu, Jie Zhang, Shufeng Wang, Yuanhong Chang, Lin Fan

المصدر: Oncology Reports.

مصطلحات موضوعية: Male, 0301 basic medicine, Cancer Research, Carcinoma, Hepatocellular, Cell, Biology, medicine.disease_cause, Mice, 03 medical and health sciences, 0302 clinical medicine, Cell Movement, Cell Line, Tumor, medicine, Animals, Humans, Annexin A2, Regulation of gene expression, Oncogene, Liver Neoplasms, RNA, General Medicine, Prognosis, Survival Analysis, Long non-coding RNA, Up-Regulation, Gene Expression Regulation, Neoplastic, MicroRNAs, 030104 developmental biology, medicine.anatomical_structure, Oncology, Tumor progression, 030220 oncology & carcinogenesis, Cancer research, Female, RNA, Long Noncoding, Carcinogenesis

الوصف: Recently, long non-coding RNA (lncRNA) FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) has been recognized to function as an oncogene in several human tumors, and FOXD2‑AS1 dysregulation has been closely associated with carcinogenesis and tumor progression. Nevertheless, the correlation between the aberrant expression of FOXD2‑AS1 and the prognosis of hepatocellular carcinoma (HCC) has not yet been elucidated. In the present study, FOXD2‑AS1 was found to be overexpressed in HCC tissues, and FOXD2‑AS1 overexpression resulted in significantly shortened patient survival. FOXD2‑AS1 overexpression enhanced the viability and metastasis of HCC cells in vitro and in vivo, as revealed by MTT, wound healing and cell migration assays. In addition, mechanistic studies revealed that FOXD2‑AS1 upregulated the expression of the miR‑206 target gene annexin A2 (ANXA2) by acting as a miR‑206 sponge. In summary, FOXD2‑AS1 was concluded to function as an oncogene in HCC and to upregulate ANXA2 expression in part by 'sponging' miR‑206.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5224fa8824903264dc14291d8e23a0b3Test
https://doi.org/10.3892/or.2018.6752Test

المؤلفون: Guangbing Wei, Xuqi Li, Yuanhong Chang, Xinming Chang, Cancan Zhou, Guanglin Qiu, Lin Fan, Guanghui Wang

المصدر: Oncology Reports.

مصطلحات موضوعية: Adult, Male, 0301 basic medicine, Cancer Research, Carcinoma, Hepatocellular, FOXO1, P70-S6 Kinase 1, Mice, 03 medical and health sciences, 0302 clinical medicine, Cell Line, Tumor, medicine, Animals, Humans, Luciferase, 3' Untranslated Regions, Protein kinase B, Transcription factor, Cell Proliferation, Oncogene, Forkhead Box Protein O1, Chemistry, Liver Neoplasms, Cancer, Hep G2 Cells, General Medicine, Middle Aged, medicine.disease, Up-Regulation, Gene Expression Regulation, Neoplastic, MicroRNAs, 030104 developmental biology, Oncology, 030220 oncology & carcinogenesis, Cancer research, Female, Liver cancer, Neoplasm Transplantation, Signal Transduction

الوصف: In the present study, we investigated whether miRNA‑300 (miR‑300) is an oncogene in human liver cancer and sought to determine the mechanism underlying its activity. We also investigated the effect of miRNA‑300 on the growth in liver cancer. To identify its target molecule, we performed luciferase assays. The downstream signaling pathway was detected by immunohistochemical (IHC) analysis in human HCC tissues, and the protein levels of AKT, 4E‑BP1, S6K1, SNAIL and MMP2 were determined using western blotting. miR‑300 levels were higher in patients with high‑stage HCC, and miR‑300 promoted cell growth both in vitro and in vivo. miRNA‑300 inhibited the luciferase activity of FOXO1 by targeting its 3'‑untranslated region (UTR), and overexpression of miR‑300 upregulated the protein levels of phospho‑AKT, phospho‑4E‑BP1, phospho‑S6K1, SNAIL and MMP2. These data revealed that miRNA‑300 functions as an oncogene in liver cancer by inhibiting FOXO1 and interacting with the AKT/mTOR signaling pathway.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1e6460d883f6168e2ef63e884f766ec8Test
https://doi.org/10.3892/or.2018.6727Test

المؤلفون: Chen-Ying Liu, Long Cui, Yuji Huang, Tingyu Wu, Zhehui Zhu, Wei Chen, Zhenyu Huang, Yun Liu, Peng Du, Yili Yang, Guanghui Wang

المصدر: Cell Death and Disease, Vol 9, Iss 3, Pp 1-13 (2018)
Cell Death & Disease

مصطلحات موضوعية: Oncogene Protein p55(v-myc), 0301 basic medicine, Cancer Research, Angiogenesis, Immunology, Mice, Nude, Antineoplastic Agents, Article, Bortezomib, Proto-Oncogene Proteins c-myc, Mice, 03 medical and health sciences, Cellular and Molecular Neuroscience, chemistry.chemical_compound, Cell Line, Tumor, medicine, Animals, Humans, lcsh:QH573-671, Gene knockdown, lcsh:Cytology, Forkhead Box Protein M1, NF-kappa B, Nuclear Proteins, Drug Synergism, NF-κB, Azepines, Cell Cycle Checkpoints, Cell Biology, Triazoles, Xenograft Model Antitumor Assays, Gene Expression Regulation, Neoplastic, CTGF, IκBα, 030104 developmental biology, chemistry, Cell culture, FOXM1, Cancer research, Female, Colorectal Neoplasms, medicine.drug

الوصف: The bromodomain and extra-terminal domain inhibitors (BETi) are promising epigenetic drugs for the treatment of various cancers through suppression of oncogenic transcription factors. However, only a subset of colorectal cancer (CRC) cells response to BETi. We investigate additional agents that could be combined with BETi to overcome this obstacle. JQ1-resistant CRC cells were used for screening of the effective combination therapies with JQ1. RNA-seq was performed to explore the mechanism of synergistic effect. The efficacy of combinational treatment was tested in the CRC cell line- and patient-derived xenograft (PDX) models. In BETi-sensitive CRC cells, JQ1 also impaired tumor angiogenesis through the c-myc/miR-17-92/CTGF+THBS1 axis. CTGF knockdown moderately counteracted anti-angiogenic effect of JQ1 and led to partially attenuated tumor regression. JQ1 decreased c-myc expression and NF-κB activity in BETi-sensitive CRC cells but not in resistant cells. Bortezomib synergistically sensitized BETi-resistant cells to the JQ1 treatment, and JQ1+Bortezomib induced G2/M arrest in CRC cells. Mechanistically, inhibition of NF-κB by Bortezomib or NF-κB inhibitor or IKK1/2 siRNA all rendered BETi-resistant cells more sensitive to BETi by synergistic repression of c-myc, which in turn induces GADD45s’ expression, and by synergistic repression of FOXM1 which in turn inhibit G2/M checkpoint genes’ expression. Activation of NF-κB by IκBα siRNA induced resistance to JQ1 in BETi-sensitive CRC cells. Last, JQ1+Bortezomib inhibited tumor growth and angiogenesis in CRC cell line xenograft model and four PDX models. Our results indicate that anti-angiogenic effect of JQ1 plays a vital role in therapeutic effect of JQ1 in CRC, and provide a rationale for combined inhibition of BET proteins and NF-κB as a potential therapy for CRC.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::98dfba00770d13875803bd1ad3fe0c09Test
https://doi.org/10.1038/s41419-018-0354-yTest

المؤلفون: Long Cui, Guanghui Wang, Hailan He, Zhenyu Huang, Ximao Cui, Wenbin Shen

المصدر: Oncology reports. 40(2)

مصطلحات موضوعية: 0301 basic medicine, Male, Cancer Research, Colorectal cancer, Mice, Nude, Lysyl oxidase, Apoptosis, Biology, Metastasis, Cell Line, 03 medical and health sciences, Mice, 0302 clinical medicine, Cell Line, Tumor, medicine, Animals, Humans, RNA, Messenger, Neoplasm Metastasis, neoplasms, Cell Proliferation, Tissue microarray, LOXL2, Oncogene, Cancer, General Medicine, Cell cycle, Middle Aged, medicine.disease, HCT116 Cells, Prognosis, digestive system diseases, Extracellular Matrix, Gene Expression Regulation, Neoplastic, 030104 developmental biology, HEK293 Cells, Oncology, 030220 oncology & carcinogenesis, Cancer research, Female, Amino Acid Oxidoreductases, Colorectal Neoplasms, HT29 Cells

الوصف: Colorectal cancer (CRC) is the third most common type of cancer. In the present study, the expression and intracellular localization of lysyl oxidase-like 2 (LOXL2) protein in CRC were examined. Quantitative polymerase chain reaction and western blot analysis of LOXL2 mRNA and protein expression was performed for 40 pairs of CRC tumor and normal mucosa tissue samples. The immunohistochemical staining of tissue microarrays was performed to detect LOXL2 protein expression. LOXL2 was highly expressed in the extracellular matrix and CRC cells. The positive expression of LOXL2 in CRC cells was significantly associated with the tumor tumor-node metastasis stage and distant metastasis, while elevated LOXL2 expression within the CRC cells was an independent prognostic factor in patients with CRC. The knockdown of LOXL2 impaired the proliferative and migratory abilities of CRC cells in vitro and in vivo, and induced cell cycle arrest and apoptosis. These findings indicated that LOXL2 might have an important role in CRC.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a19bd73c8503009f4308d8ed9dda59f0Test
https://pubmed.ncbi.nlm.nih.gov/29845296Test

المؤلفون: Elizabeth Murphy, Marjan Gucek, Guanghui Wang, Sara Menazza, Tiffany Nguyen, Renee Wong

المصدر: Journal of Molecular and Cellular Cardiology. 56:81-90

مصطلحات موضوعية: Male, Proteome, Citric Acid Cycle, Mitochondrion, Mitochondrial Membrane Transport Proteins, Article, Mitochondria, Heart, Mitochondrial Proteins, Cyclophilins, Mice, Mitochondrial membrane transport protein, chemistry.chemical_compound, Oxygen Consumption, Pyruvic Acid, Animals, Molecular Biology, Heart metabolism, Mice, Knockout, biology, Mitochondrial Permeability Transition Pore, Myocardium, MPTP, Succinate dehydrogenase, Metabolism, Citric acid cycle, Biochemistry, chemistry, Mitochondrial permeability transition pore, biology.protein, Female, Propionates, Cardiology and Cardiovascular Medicine, Amino Acids, Branched-Chain, Cyclophilin D

الوصف: Cyclophilin D (CypD) is a mitochondrial chaperone that has been shown to regulate the mitochondrial permeability transition pore (MPTP). MPTP opening is a major determinant of mitochondrial dysfunction and cardiomyocyte death during ischemia/reperfusion (I/R) injury. Mice lacking CypD have been widely used to study regulation of the MPTP, and it has been shown recently that genetic depletion of CypD correlates with elevated levels of mitochondrial Ca(2+). The present study aimed to characterize the metabolic changes in CypD(-/-) hearts. Initially, we used a proteomics approach to examine protein changes in CypD(-/-) mice. Using pathway analysis, we found that CypD(-/-) hearts have alterations in branched chain amino acid metabolism, pyruvate metabolism and the Krebs cycle. We tested whether these metabolic changes were due to inhibition of electron transfer from these metabolic pathways into the electron transport chain. As we found decreased levels of succinate dehydrogenase and electron transfer flavoprotein in the proteomics analysis, we examined whether activities of these enzymes might be altered. However, we found no alterations in their activities. The proteomics study also showed a 23% decrease in carnitine-palmitoyltransferase 1 (CPT1), which prompted us to perform a metabolomics analysis. Consistent with the decrease in CPT1, we found a significant decrease in C4/Ci4, C5-OH/C3-DC, C12:1, C14:1, C16:1, and C20:3 acyl carnitines in hearts from CypD(-/-) mice. In summary, CypD(-/-) hearts exhibit changes in many metabolic pathways and caution should be used when interpreting results from these mice as due solely to inhibition of the MPTP.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b1e22876228ee80d33b2511dc831f562Test
https://doi.org/10.1016/j.yjmcc.2012.12.004Test

المؤلفون: Fredrick W. Alt, Marjan Gucek, Elizabeth Murphy, Guanghui Wang, Guang Tong, In Hye Lee, Renee Wong, Ilsa I. Rovira, Nisha Narayan, Jie Liu, Ronen Borenstein, Toren Finkel, Hwei Ling Cheng, Michael N. Sack, Junhui Sun, Maria M. Fergusson, Liu Cao, David B. Lombard

المصدر: Nature. 492:199-204

مصطلحات موضوعية: Male, Necrosis, Regulator, Biology, SIRT2, Jurkat cells, Article, Cell Line, Jurkat Cells, Mice, Sirtuin 2, medicine, Animals, Humans, Gene knockdown, Multidisciplinary, HEK 293 cells, Acetylation, Molecular biology, Cell biology, Nuclear Pore Complex Proteins, HEK293 Cells, Receptor-Interacting Protein Serine-Threonine Kinases, Female, Tumor necrosis factor alpha, medicine.symptom, HeLa Cells, Protein Binding

الوصف: Although initially viewed as unregulated, increasing evidence suggests that cellular necrosis often proceeds through a specific molecular program. In particular, death ligands such as tumour necrosis factor (TNF)-α activate necrosis by stimulating the formation of a complex containing receptor-interacting protein 1 (RIP1) and receptor-interacting protein 3 (RIP3). Relatively little is known regarding how this complex formation is regulated. Here, we show that the NAD-dependent deacetylase SIRT2 binds constitutively to RIP3 and that deletion or knockdown of SIRT2 prevents formation of the RIP1-RIP3 complex in mice. Furthermore, genetic or pharmacological inhibition of SIRT2 blocks cellular necrosis induced by TNF-α. We further demonstrate that RIP1 is a critical target of SIRT2-dependent deacetylation. Using gain- and loss-of-function mutants, we demonstrate that acetylation of RIP1 lysine 530 modulates RIP1-RIP3 complex formation and TNF-α-stimulated necrosis. In the setting of ischaemia-reperfusion injury, RIP1 is deacetylated in a SIRT2-dependent fashion. Furthermore, the hearts of Sirt2(-/-) mice, or wild-type mice treated with a specific pharmacological inhibitor of SIRT2, show marked protection from ischaemic injury. Taken together, these results implicate SIRT2 as an important regulator of programmed necrosis and indicate that inhibitors of this deacetylase may constitute a novel approach to protect against necrotic injuries, including ischaemic stroke and myocardial infarction.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0a6c6faac3cede9a1675100ae91f9ca9Test
https://doi.org/10.1038/nature11700Test

المؤلفون: Lei, Xie, Fuquan, Jiang, Xindao, Zhang, Gulimiran, Alitongbieke, Xinlei, Shi, MinJun, Meng, Yiming, Xu, Anshi, Ren, Jing, Wang, Lijun, Cai, Yunxia, Zhou, Yang, Xu, Ying, Su, Jie, Liu, Zhiping, Zeng, Guanghui, Wang, Hu, Zhou, Quan Cheng, Chen, Xiao-Kun, Zhang

المصدر: British journal of pharmacology. 173(2)

مصطلحات موضوعية: Mice, Inbred BALB C, Tumor Necrosis Factor-alpha, Biphenyl Compounds, Mice, Nude, Apoptosis, Breast Neoplasms, Hep G2 Cells, Xenograft Model Antitumor Assays, Research Papers, Lignans, Gene Expression Regulation, Neoplastic, Mice, MCF-7 Cells, Nuclear Receptor Subfamily 4, Group A, Member 1, Animals, Humans, Female, Drugs, Chinese Herbal, HeLa Cells

الوصف: The orphan nuclear receptor Nur77 is implicated in the survival and apoptosis of cancer cells. The purpose of this study was to determine whether and how Nur77 serves to mediate the effect of the inflammatory cytokine TNF-α in cancer cells and to identify and characterize new agents targeting Nur77 for cancer therapy.The effects of TNF-α on the expression and function of Nur77 were studied using in vitro and in vivo models. Nur77 expression was evaluated in tumour tissues from breast cancer patients. The anticancer effects of honokiol and its mechanism of action were assessed by in vitro, cell-based and animal studies.TNF-α rapidly and potently induced the expression of Nur77 in breast cancer cells through activation of IκB kinase and JNK. Knocking down Nur77 resulted in TNF-α-dependent apoptosis, while ectopic Nur77 expression in MCF-7 cells promoted their growth in animals. Levels of Nur77 were higher in tumour tissues than the corresponding tissues surrounding the tumour in about 50% breast cancer patients studied. Our in vitro and animal studies also identified honokiol as an effective sensitizer of TNF-α-induced apoptosis by inhibiting TNF-α-induced Nur77 mRNA expression, which could be attributed to its interference of TNFR1's interaction with receptor-interacting protein 1 (RIPK1).TNF-α-induced Nur77 serves as a survival factor to attenuate the death effect of TNF-α in cancer cells. With its proven human safety profile, honokiol represents a promising agent that warrants further clinical development.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=pmid________::e77376195d7c519d3e506b802cee549fTest
https://pubmed.ncbi.nlm.nih.gov/26505879Test