作者机构：
[Chen, Kaiqin; Liang, Junjie; Lu, Fangguo; Wei, Ke; Ye, Chun; Gao, Zihan] Hunan Univ Chinese Med, Med Sch, Changsha 410208, Peoples R China.;[Wei, Ke] Hunan Univ Chinese Med, Hunan Prov Key Lab Integrat Pathogen Biol, Changsha 410208, Hunan, Peoples R China.
通讯机构：
[Wei, K ] H;Hunan Univ Chinese Med, Med Sch, Changsha 410208, Peoples R China.;Hunan Univ Chinese Med, Hunan Prov Key Lab Integrat Pathogen Biol, Changsha 410208, Hunan, Peoples R China.
关键词：
miRNA;lncRNA;circRNA;Breast cancer cells;Glucose metabolism
摘要：
Breast cancer is the tumor with the highest incidence in women worldwide. According to research, the poor prognosis of breast cancer is closely related to abnormal glucose metabolism in tumor cells. Changes in glucose metabolism in tumor cells are an important feature. When sufficient oxygen is available, cancer cells tend to undergo glycolysis rather than oxidative phosphorylation, which promotes rapid proliferation and invasion of tumor cells. As research deepens, targeting the glucose metabolism pathway of tumor cells is seen as a promising treatment. Non-coding RNAs (ncRNAs), a recent focus of research, are involved in the regulation of enzymes of glucose metabolism and related cancer signaling pathways in breast cancer cells. This article reviews the regulatory effect and mechanism of ncRNAs on glucose metabolism in breast cancer cells and provides new ideas for the treatment of breast cancer.
作者：
Zhou, Feng;Zhang, Guo Dong;Tan, Yang;Hu, Shi An;Tang, Qun*;...
期刊：
Therapeutic Advances in Gastroenterology,2023年16:17562848231176889 ISSN：1756-283X
通讯作者：
Tang, Qun;Pei, G;Tang, Q
作者机构：
[Tang, Qun; Zhou, Feng; Tang, Q; Pei, G; Pei, Gang] Hunan Univ Chinese Med, Sch Pharm, Changsha 410208, Peoples R China.;[Tang, Qun; Tang, Q] Hunan Univ Chinese Med, Med Sch, Changsha, Peoples R China.;[Zhou, Feng; Pei, G; Pei, Gang] Educ Dept Hunan Prov, Key Lab Modern Res TCM, Changsha, Peoples R China.;[Zhang, Guo Dong] Ningxia Med Univ, Yinchuan, Ningxia, Peoples R China.;[Tan, Yang; Hu, Shi An] Hunan Univ Chinese Med, Sch Pharm, Changsha, Peoples R China.
通讯机构：
[Tang, Q; Pei, G ; Tang, Q ] H;Hunan Univ Chinese Med, Sch Pharm, Changsha 410208, Peoples R China.;Hunan Univ Chinese Med, Med Sch, Changsha, Peoples R China.;Educ Dept Hunan Prov, Key Lab Modern Res TCM, Changsha, Peoples R China.
摘要：
Therapeutic Advances in Gastroenterology, Volume 16, Issue , January-December 2023. <br/>Inflammatory bowel disease (IBD) is a chronic gastrointestinal inflammatory disease that involves host genetics, the microbiome, and inflammatory responses. The current consensus is that the disruption of the intestinal mucosal barrier is the core pathogenesis of IBD, including intestinal microbial factors, abnormal immune responses, and impaired intestinal mucosal barrier. Cumulative data show that nucleotide-binding and oligomerization domain (NOD)-like receptors (NLRs) are dominant mediators in maintaining the homeostasis of the intestinal mucosal barrier, which play critical roles in sensing the commensal microbiota, maintaining homeostasis, and regulating intestinal inflammation. Blocking NLRs inflammasome activation by botanicals may be a promising way to prevent IBD progression. In this review, we systematically introduce the multiple roles of NLRs in regulating intestinal mucosal barrier homeostasis and focus on summarizing the activities and potential mechanisms of natural products against IBD. Aiming to propose new directions on the pathogenesis and precise treatment of IBD
期刊：
Cancer Cell International,2023年23(1):1-15 ISSN：1475-2867
通讯作者：
Sheng, W;Li, YQ
作者机构：
[Xu, Wenjing] Hunan Univ Chinese Med, Affiliated Hosp 1, Dept Dermatol, Changsha 410021, Peoples R China.;[Ding, Jin] Guangzhou Univ Chinese Med, Shenzhen Baoan Tradit Chinese Med Hosp, Dept Androl, Shenzhen 518133, Peoples R China.;[Li, Bonan; Sheng, W; Sheng, Wen; Kuang, Shida; Zhu, Congxu; Sun, Tiansong] Hunan Univ Chinese Med, Androl Lab, Changsha 410208, Peoples R China.;[Kuang, Shida] Hunan Univ Chinese Med, Sch Tradit Chinese Med, Changsha 410208, Peoples R China.;[Li, Bonan; Sheng, W; Sheng, Wen; Zhu, Congxu; Sun, Tiansong] Hunan Univ Chinese Med, Sch Integrated Chinese & Western Med, Changsha 410208, Peoples R China.
通讯机构：
[Sheng, W ; Li, YQ ] H;Hunan Univ Chinese Med, Androl Lab, Changsha 410208, Peoples R China.;Hunan Univ Chinese Med, Sch Integrated Chinese & Western Med, Changsha 410208, Peoples R China.;Hunan Univ Chinese Med, Med Sch, Changsha 410208, Peoples R China.
摘要：
Docetaxel (DTX) resistance reduces therapeutic efficacy in prostate cancer (PCa). Accumulating reports support the role of phytochemicals in the reversal of DTX resistance. This study aimed to determine whether Epimedium brevicornu and Curcuma zedoaria extracts (ECe), specially icariin-curcumol, attenuates DTX resistance and explore their potential mechanisms. Regulatory pathways were predicted between ECe active ingredients and PCa using network pharmacology. DTX-resistant cell LNCaP/R were established based on DTX-sensitive LNCaP, and xenograft models were further established. Active ingredients in ECe by HLPC-MS were identified. The binding of icariin and curcumol to the target was analyzed by molecular docking. Biochemical experiments were applied to determine the possible mechanisms by which Icariin-Curcumol regulates DTX sensitivity. Akt1 and the PI3K-Akt signaling pathway were predicted as the primary functional target between drug and PCa. ECe and DTX inhibited xenograft tumor growth, inflammation, cell viability and promoted apoptosis. Icariin and curcumol were detected in ECe, and icariin and curcumol docked with Akt1. ECe, Icariin-Curcumol and DTX downregulated AR, PSA, PI3K, Akt1, mTOR, and HIF-1ɑ. Moreover, ECe, Icariin-Curcumol and DTX increased glucose and PDH, decreased lactic acid, ATP and LDH, and downregulated c-Myc, hnRNPs, VEGF, PFK1, and PKM2. Notably, the anti-PCa effect of DTX was attenuated compared to ECe or Icariin-Curcumol in the LNCaP/R model. The combined effect of Icariin-Curcumol and DTX was superior to that of DTX. Our data support that Icariin-Curcumol reverses DTX resistance by inhibiting the PI3K-Akt signaling and the Warburg effect, providing new ideas for improving therapeutic measures for PCa.
摘要：
BackgroundForkhead box M1 (FOXM1) is a member of the Forkhead box (Fox) transcription factor family. It regulates cell mitosis, cell proliferation, and genome stability. However, the relationship between the expression of FOXM1 and the levels of m6a modification, immune infiltration, glycolysis, and ketone body metabolism in HCC has yet to be fully elucidated. MethodsTranscriptome and somatic mutation profiles of HCC were downloaded from the TCGA database. Somatic mutations were analyzed by maftools R package and visualized in oncoplots. GO, KEGG and GSEA function enrichment was performed on FOXM1 co-expression using R. We used Cox regression and machine learning algorithms (CIBERSORT, LASSO, random forest, and SVM-RFE) to study the prognostic value of FOXM1 and immune infiltrating characteristic immune cells in HCC. The relationship between FOXM1 and m6A modification, glycolysis, and ketone body metabolism were analyzed by RNA-seq and CHIP-seq. The competing endogenous RNA (ceRNA) network construction relies on the multiMiR R package, ENCORI, and miRNET platforms. ResultsFOXM1 is highly expressed in HCC and is associated with a poorer prognosis. At the same time, the expression level of FOXM1 is significantly related to the T, N, and stage. Subsequently, based on the machine learning strategies, we found that the infiltration level of T follicular helper cells (Tfh) was a risk factor affecting the prognosis of HCC patients. The high infiltration of Tfh was significantly related to the poor overall survival rate of HCC. Besides, the CHIP-seq demonstrated that FOXM1 regulates m6a modification by binding to the promoter of IGF2BP3 and affects the glycolytic process by initiating the transcription of HK2 and PKM in HCC. A ceRNA network was successfully obtained, including FOXM1 - has-miR-125-5p - DANCR/MIR4435-2HG ceRNA network related to the prognosis of HCC. ConclusionOur study implicates that the aberrant infiltration of Tfh associated with FOXM1 is a crucial prognostic factor for HCC patients. FOXM1 regulates genes related to m6a modification and glycolysis at the transcriptional level. Furthermore, the specific ceRNA network can be used as a potential therapeutic target for HCC.
摘要：
Respiratory diseases are an emerging public health concern, that pose a risk to the global community. There, it is essential to establish effective treatments to reduce the global burden of respiratory diseases. Astragaloside IV (AS-IV) is a natural saponin isolated from Radix astragali (Huangqi in Chinese) used for thousands of years in Chinese medicine. This compound has become increasingly popular due to its potential anti-inflammatory, antioxidant, and anticancer properties. In the last decade, accumulated evidence has indicated the AS-IV protective effect against respiratory diseases. This article presents a current understanding of AS-IV roles and mechanisms in combatting respiratory diseases. The ability of the agent to suppress oxidative stress, cell proliferation, and epithelial-mesenchymal transition (EMT), to attenuate inflammatory responses, and modulate programmed cell death (PCD) will be discussed. This review highlights the current challenges in respiratory diseases and recommendations to improve disease management.
摘要：
Ferroptosis has been observed during retinal photoreceptor cell death, suggesting that it plays a role in retinitis pigmentosa (RP) pathogenesis. Qi-Shen-Tang (QST) is a combination of two traditional Chinese medicines used for the treatment of ophthalmic diseases; however, its mechanism of action in RP and ferroptosis remains unclear. Therefore, this study aimed to explore the effect and potential molecular mechanisms of QST on RP. QST significantly improved tissue morphology and function of the retina in the RP model mice. A significant increase in retinal blood flow and normalization of the fundus structure were observed in mice in the treatment group. After QST treatment, the level of iron and the production of malondialdehyde decreased significantly; the levels of superoxide dismutase and glutathione increased significantly; and the protein expression of glutathione peroxidase 4 (GPX4), glutathione synthetase, solute carrier family 7 member 11, and nuclear factor erythroid 2-related factor 2 (NRF2) increased significantly. The molecular docking results demonstrated potential interactions between the small molecules of QST and the key proteins of NRF2/GPX4 signaling pathway. Our results indicate that QST may inhibit ferroptosis by inhibiting the NRF2/GPX4 signaling pathway, thereby reducing RP-induced damage to retinal tissue.
作者：
Liu, Yong-Ping;Lei, Jian;Yin, Ming-Ming;Chen, Yi
期刊：
Anti-Cancer Agents in Medicinal Chemistry,2022年22(13):2448-2457 ISSN：1871-5206
通讯作者：
Liu, Y.-P.
作者机构：
[Chen, Yi; Liu, Yong-Ping] Hunan Univ Chinese Med, Sch Med, Dept Physiol, 300 Xueshi Rd,Hanpu Sci & Educ Pk, Changsha 410208, Hunan, Peoples R China.;[Lei, Jian] Hunan Univ, Coll Chem & Chem Engn, State Key Lab Chemo Biosensing & Chemometr, Changsha 410082, Hunan, Peoples R China.;[Yin, Ming-Ming] Hunan Univ Chinese Med, Coll Integrated Tradit Chinese & Western Med, Changsha 410208, Hunan, Peoples R China.
通讯机构：
Department of Physiology, School of Medicine, Hunan University of Chinese Medicine, 300 Xueshi Road, Hanpu Science and Education Park, Yuelu District Hunan, Changsha, China
关键词：
Metal complex;necroptosis inducer;anti-cancer;triple-negative breast cancer;ROS;oxidative stress.
摘要：
Aim: This study aimed to investigate the anticancer effect and the underlying mechanisms of organoantimony (III) fluoride on MDA-MB-231 human breast cancer cells. Methods: Five cancer and one normal cell line were treated with an organoantimony (III) compound 6-cyclohexyl-12- fluoro-5,6,7,12-tetrahydrodibenzo[c,f][1,5]azastibocine (denoted as C4). The cell viability was detected by MTT assay. Induction of cell death was determined by Hoechst 33342/PI staining and Annexin-V/PI staining. The effect of C4 on the necroptotic relative protein was determined by Western blot analysis. Results: Among the five cancer cell lines, C4 decreased the viability of MDA-MB-231, MCF-7 and A2780/cisR, and showed less toxicity on normal human embryonic kidney cells. In breast cancer cell line MDA-MB-231, the C4 treatment induced necrotic cell death as well as LDH release in a time- and dose-dependent manner. Moreover, C4 could increase the expression of phosphorylated RIPK3 and MLKL proteins. Overall, the C4 treatment resulted in the reduction of mitochondrial transmembrane potential and accumulation of ROS in MDA-MB-231 cells. Conclusion: C4-induced necroptosis could be ascribed to glutathione depletion and ROS elevation in MDA-MB-231 cells. Our findings illustrate C4 to be a potential necroptosis inducer for breast cancer treatment.
摘要：
The circadian rhythm is an endogenous clock system that coordinates and optimizes various physiological and pathophysiological processes, which accord with the master and the peripheral clock. Increasing evidence indicates that endogenous circadian rhythm disruption is involved in the lesion volume and recovery of ischemic stroke. As a critical recovery mechanism in post-stroke, angiogenesis reestablishes the regional blood supply and enhances cognitive and behavioral abilities, which is mainly composed of the following processes: endothelial cell proliferation, migration, and pericyte recruitment. The available evidence revealed that the circadian governs many aspects of angiogenesis. This study reviews the mechanism by which circadian rhythms regulate the process of angiogenesis and its contribution to functional recovery in post-stroke at the aspects of the molecular level. A comprehensive understanding of the circadian clock regulating angiogenesis in post-stroke is expected to develop new strategies for the treatment of cerebral infarction.
作者机构：
[Chen, Keke; Zhou, Ji; Dong, Jun; He, Qizhi; Chen, Danna; Ma, Shuheng; Wang, Jingya] Changsha Med Univ, Academician Workstn, Changsha 410219, Hunan, Peoples R China.;[Ning, Yi] Hunan Univ Chinese Med, Dept Microbiol, Med Sch, Changsha 410208, Hunan, Peoples R China.;[Zhou, Ji; He, Qizhi; Chen, Danna] Changsha Med Univ, Sch Basic Med Sci, Changsha, Hunan, Peoples R China.;[Dong, Jun; He, Qizhi; Ma, Shuheng] Changsha Med Univ, Discipline Basic Med Applicat, Changsha, Hunan, Peoples R China.
通讯机构：
[Danna Chen] A;[Yi Ning] D;Academician Workstation, Changsha Medical University, Changsha, Hunan, People’s Republic of China<&wdkj&>School of Basic Medical Science, Changsha Medical University, Changsha, Hunan, People’s Republic of China<&wdkj&>Department of Microbiology, The Medicine School of Hunan University of Chinese Medicine, Changsha, Hunan, People’s Republic of China
期刊：
Drug Delivery,2022年29(1):1675-1683 ISSN：1071-7544
通讯作者：
Fangguo Lu
作者机构：
[Chen, Pingan; Ning, Yi; Wang, Xiaoqi; Lu, Fangguo; Hu, Jue; Xiao, Rong; Liu, Shiwu] Hunan Univ Chinese Med, Med Sch, Dept Microbiol, Changsha 410208, Hunan, Peoples R China.;[Li, Ling] Hunan Univ Chinese Med, Chinese Med Sch, Expt Ctr Mol Biol, Changsha, Hunan, Peoples R China.
通讯机构：
[Fangguo Lu] D;Department of Microbiology, The Medicine School of Hunan University of Chinese Medicine, Changsha, Hunan, People’s Republic of China
作者机构：
The First Hospital of Hunan University of Chinese Medicine, Hunan University of Chinese Medicine;College of Integrated Chinese and Western Medicine, Hunan Key Laboratory of Translational Research in Formulas and Zheng of Traditional Chinese Medicine, Hunan University of Chinese Medicine;Department of Preventive Dentistry, Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou Medical University;Department of Physiology, Hunan University of Chinese Medicine;State Key Laboratory of Quality Research in Chinese Medicine, Macau Institute For Applied Research in Medicine and Health, Macau University of Science and Technology
关键词：
Hepatocellular carcinoma;Xihuang pills;Apoptosis;Antitumour;Phosphoinositide 3-kinase/protein kinase-B/mechanistic target of rapamycin pathway
摘要：
BACKGROUND The phosphoinositide 3-kinase/protein kinase-B/mechanistic target of rapamycin（PI3K/Akt/mTOR） signalling pathway is crucial for cell survival, differentiation, apoptosis and metabolism. Xihuang pills（XHP） are a traditional Chinese preparation with antitumour properties. They inhibit the growth of breast cancer, glioma, and other tumours by regulating the PI3K/Akt/mTOR signalling pathway. However, the effects and mechanisms of action of XHP in hepatocellular carcinoma（HCC） remain unclear. Regulation of the PI3K/Akt/mTOR signalling pathway effectively inhibits the progression of HCC. However, no study has focused on the XHPassociated PI3K/Akt/mTOR signalling pathway. Therefore, we hypothesized that XHP might play a role in inhibiting HCC through the PI3K/Akt/mTOR signalling pathway.AIM To confirm the effect of XHP on HCC and the possible mechanisms involved.METHODS The chemical constituents and active components of XHP were analysed using ultra-performance liquid chromatography-quadrupole time of flight mass spectrometry（UPLC-Q-TOF-MS）. Cellbased experiments and in vivo xenograft tumour experiments were utilized to evaluate the effect of XHP on HCC tumorigenesis. First, SMMC-7721 cells were incubated with different concentrations of XHP（0, 0.3125, 0.625, 1.25, and 2.5 mg/mL） for 12 h, 24 h and 48 h. Cell viability was assessed using the CCK-8 assay, followed by an assessment of cell migration using a wound healing assay.Second, the effect of XHP on the apoptosis of SMMC-7721 cells was evaluated. SMMC-7721 cells were stained with fluorescein isothiocyanate and annexin V/propidium iodide. The number of apoptotic cells and cell cycle distribution were measured using flow cytometry. The cleaved protein and mRNA expression levels of caspase-3 and caspase-9 were detected using Western blotting and quantitative reverse-transcription polymerase chain reaction（RT-qPCR）, respectively.Third, Western blotting and RT–qPCR were performed to confirm the effects of XHP on the protein and mRNA expression of components of the PI3K/Akt/mTOR signalling pathway.Finally, the effects of XHP on the tumorigenesis of subcutaneous hepatocellular tumours in nude mice were assessed.RESULTS The following 12 compounds were identified in XHP using high-resolution mass spectrometry:Valine, 4-gingerol, myrrhone, ricinoleic acid, glycocholic acid, curzerenone, 11-keto-β-boswellic acid, oleic acid, germacrone, 3-acetyl-9,11-dehydro-β-boswellic acid, 5β-androstane-3,17-dione, and 3-acetyl-11-keto-β-boswellic acid. The cell viability assay results showed that treatment with 0.625mg/mL XHP extract decreased HCC cell viability after 12 h, and the effects were dose-and timedependent. The results of the cell scratch assay showed that the migration of HCC cells was significantly inhibited in a time-dependent manner by the administration of XHP extract（0.625mg/mL）. Moreover, XHP significantly inhibited cell migration and resulted in cell cycle arrest and apoptosis. Furthermore, XHP downregulated the PI3K/Akt/mTOR signalling pathway, which activated apoptosis executioner proteins（e.g., caspase-9 and caspase-3）. The inhibitory effects of XHP on HCC cell growth were determined in vivo by analysing the tumour xenograft volumes and weights.CONCLUSION XHP inhibited HCC cell growth and migration by stimulating apoptosis via the downregulation of the PI3K/Akt/mTOR signalling pathway, followed by the activation of caspase-9 and caspase-3.Our findings clarified that the antitumour effects of XHP on HCC cells are mediated by the PI3K/Akt/mTOR signalling pathway, revealing that XHP may be a potential complementary therapy for HCC.
期刊：
Drug Design, Development and Therapy,2022年16:1621-1645 ISSN：1177-8881
通讯作者：
Qinhui Tuo
作者机构：
[Sun, Taoli; He, Chaoping; Quan, Wenjuan; Peng, Sha] Hunan Univ Chinese Med, Sch Pharm, Changsha 410208, Peoples R China.;[Chen, Yu; Hu, Bo; Tuo, Qinhui; Yang, Dongmei] Hunan Univ Chinese Med, Sch Med, Changsha 410208, Peoples R China.;[Liu, Jiaqin] Cent South Univ, Xiangya Hosp 1, Dept Pharm, Changsha 410011, Hunan, Peoples R China.;[Tuo, Qinhui] Hunan Univ Chinese Med, First Hosp, Changsha 410007, Peoples R China.
通讯机构：
[Qinhui Tuo] S;School of Medicine, Hunan University of Chinese Medicine, Changsha, 410208, People’s Republic of China<&wdkj&>The First hospital of Hunan University of Chinese Medicine, Changsha, 410007, People’s Republic of China
关键词：
Huo Luo Xiao Ling Dan;atherosclerosis;network pharmacology;molecular docking;molecular dynamics simulation;dihydrotanshinone I;STAT3;MAPK signaling pathway
摘要：
Nonsmall-cell lung carcinoma (NSCLC) is one of the deadliest malignancies in the world. LncRNAs are confirmed to be involved in the progression of NSCLC. Meanwhile, lncRNA CRNDE is known to be upregulated in NSCLC; however, the mechanism by which CRNDE regulates the tumourigenesis of NSCLC remains unclear. To test the function of CRNDE in NSCLC, cell proliferation, invasion, and migration were investigated by colony formation and Transwell assays, respectively. qPCR and Western blotting were applied to test gene and protein levels. In addition, the relationship among CRNDE, miR-455-3p, and HDAC2 was explored by dual-luciferase and RIP assays. The data revealed that the expression of CRNDE was upregulated in NSCLC tissues, while miR-455-3p was downregulated. CRNDE knockdown inhibited the viability, migration and invasion of NSCLC cells or epidermal growth factor receptor gene (EGFR)-mutant NSCLC cells. Moreover, inhibition of miR-455-3p exhibited the opposite effect. CRNDE bound with miR-455-3p, and HDAC2 was found to be targeted by miR-455-3p. Meanwhile, miR-455-3p downregulation reversed the effect of CRNDE knockdown on NSCLC cell function. Furthermore, miR-455-3p notably inhibited the growth and invasion of NSCLC cells via downregulation of HDAC2. Knockdown of CRNDE attenuated NSCLC progression via modulation of the miR-455-3p/HDAC2 axis. Thus, those findings might provide a novel strategy against NSCLC.
摘要：
Accumulating evidence suggests that astrocytes, the abundant cell type in the central nervous system (CNS), play a critical role in maintaining the immune response after cerebral infarction, regulating the blood-brain barrier (BBB), providing nutrients to the neurons, and reuptake of glutamate. The circadian clock is an endogenous timing system that controls and optimizes biological processes. The central circadian clock and the peripheral clock are consistent, controlled by various circadian components, and participate in the pathophysiological process of astrocytes. Existing evidence shows that circadian rhythm controls the regulation of inflammatory responses by astrocytes in ischemic stroke (IS), regulates the repair of the BBB, and plays an essential role in a series of pathological processes such as neurotoxicity and neuroprotection. In this review, we highlight the importance of astrocytes in IS and discuss the potential role of the circadian clock in influencing astrocyte pathophysiology. A comprehensive understanding of the ability of the circadian clock to regulate astrocytes after stroke will improve our ability to predict the targets and biological functions of the circadian clock and gain insight into the basis of its intervention mechanism.
