Chinese Journal of Physiology最新文献

{"title":"A glutamatergic pathway between the medial habenula and the rostral ventrolateral medulla may regulate cardiovascular function in a rat model of post-traumatic stress disorder.","authors":"Ya-Yang Wu,&nbsp;Cheng-Hong Zeng,&nbsp;Kun-Yi Cai,&nbsp;Chao Zheng,&nbsp;Meng-Ya Wang,&nbsp;Huan-Huan Zhang","doi":"10.4103/cjop.CJOP-D-23-00003","DOIUrl":"10.4103/cjop.CJOP-D-23-00003","url":null,"abstract":"<p><p>Post-traumatic stress disorder (PTSD) is a serious psychiatric disorder, and there is an association between it and the development of cardiovascular disease. The aim of this study was to explore whether there is a glutamatergic pathway connecting the medial habenula (MHb) with the rostral ventrolateral medulla (RVLM) that is involved in the regulation of cardiovascular function in a rat model of PTSD. Vesicular glutamate transporter 2 (VGLUT2)-positive neurons in the MHb region were retrogradely labeled with FluoroGold (FG) by the double-labeling technique of VGLUT2 immunofluorescence and FG retrograde tracing. Rats belonging to the PTSD model group were microinjected with artificial cerebrospinal fluid (ACSF) or kynurenic acid (KYN; a nonselective glutamate receptor blocker) into their RVLM. Subsequently, with electrical stimulation of MHb, the discharge frequency of the RVLM neurons, heart rate, and blood pressure were found to be significantly increased after microinjection of ACSF using an in vivo multichannel synchronous recording technology; however, this effect was inhibited by injection of KYN. The expression of N-methyl-D-aspartic acid (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunits was significantly increased in RVLM of PTSD model rats analyzed by the Western blotting technique. These findings suggest that there may be a glutamatergic pathway connection between MHb and RVLM and that this pathway may be involved in the regulation of cardiovascular function in the PTSD model rats, by acting on NMDA and AMPA receptors in the RVLM.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70707421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Daylily (<i>Hemerocallis fulva</i> Linn.) flowers improve sleep quality in human and reduce nitric oxide and interleukin-6 production in macrophages.","authors":"Li-Min Hsu, Hua-Wei Chen, Po-Ching Wu, Kuo-Feng Hua","doi":"10.4103/cjop.CJOP-D-23-00043","DOIUrl":"10.4103/cjop.CJOP-D-23-00043","url":null,"abstract":"<p><p>The flowers of daylily (Hemerocallis fulva Linn.) have been used as vegetable and medicinal herb for thousands of years in Taiwan and eastern Asia. Daylily flowers have been demonstrated to exert several biomedical properties. In this study, we provided the evidences show that daylily flowers exert anti-inflammatory activity in vitro and improved the sleep quality in vivo. We demonstrated that adult volunteers received water extract of daylily flowers improved sleep quality, sleep efficiency and daytime functioning, while sleep latency was reduced, compared to the adult volunteers received water. In addition, we demonstrated that aqueous and ethanol extracts of daylily flowers inhibited nitric oxide and interleukin-6 production in lipopolysaccharide-activated macrophages. Furthermore, the quantitative high performance liquid chromatography-based analysis showed the rutin content of the aqueous extract, ethanolic extract, ethyl acetate fractions of ethanolic extract, and water fractions of ethanolic extract were 7.27, 23.30, 14.71, and 57.43 ppm, respectively. These results indicate that daylily flowers have the potential to be a nutraceutical for improving inflammatory-related diseases and sleep quality in the future.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71478666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Partner of NOB1 homolog transcriptionally activated by E2F transcription factor 1 promotes the malignant progression and inhibits ferroptosis of pancreatic cancer.","authors":"Qin Yang, Bin Yang, Min Chen","doi":"10.4103/cjop.CJOP-D-23-00063","DOIUrl":"10.4103/cjop.CJOP-D-23-00063","url":null,"abstract":"<p><p>Pancreatic cancer (PC) is one of the deadliest malignancies. Partner of NOB1 homolog (PNO1) has been reported to be involved in tumorigenesis. However, the role of PNO1 in PC remains to be elucidated. The purpose of this study was to examine the effects of PNO1 on the progression of PC and the possible mechanism related to E2F transcription factor 1 (E2F1), a transcription factor predicted by the JASPAR database to bind to the PNO1 promoter region and promoted the proliferation of pancreatic ductal adenocarcinoma. First, PNO1 expression in PC tissues and its association with survival rate were analyzed by the Gene Expression Profiling Interactive Analysis database. Western blot and reverse transcription-quantitative polymerase chain reaction were used to evaluate PNO1 expression in several PC cell lines. After PNO1 silencing, cell proliferation, migration, and invasion were measured by colony formation assay, 5-ethynyl-2'-deoxyuridine staining, wound healing, and transwell assays. Then, the lipid reactive oxygen species in PANC-1 cells was estimated by using C11-BODIPY^581/591 probe. The levels of glutathione, malondialdehyde, and iron were measured. The binding between PNO1 and E2F1 was confirmed by luciferase and chromatin immunoprecipitation (ChIP) assays. Subsequently, E2F1 was overexpressed in PANC-1 cells with PNO1 knockdown to perform the rescue experiments. Results revealed that PNO1 was highly expressed in PC tissues and PNO1 expression was positively correlated with overall survival rate and disease-free survival rate. Significantly elevated PNO1 expression was also observed in PC cell lines. PNO1 knockdown inhibited the proliferation, migration, and invasion of PANC-1 cells. Moreover, ferroptosis was promoted in PNO1-silenced PANC-1 cells. Results of luciferase and ChIP assays indicated that E2F1 could bind to PNO1 promoter region. Rescue experiments suggested that E2F1 overexpression reversed the impacts of PNO1 depletion on the malignant behaviors and ferroptosis in PANC-1 cells. Summing up, PNO1 transcriptionally activated by E2F1 promotes the malignant progression and inhibits the ferroptosis of PC.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71478669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ZWINT promotes the proliferation, migration, and invasion of cervical cancer cells by regulating the p53/p21 signaling pathway.","authors":"Zhe Ma,&nbsp;Yufei Cai,&nbsp;Chenchen Tian","doi":"10.4103/cjop.CJOP-D-23-00001","DOIUrl":"10.4103/cjop.CJOP-D-23-00001","url":null,"abstract":"<p><p>Cervical cancer leads to 300,000 deaths annually and the mechanism of cervical carcinogenesis remains unclear. Zeste White 10-interacting kinetochore protein (ZWINT) is uniquely elevated in malignancies, promoting proliferation, migration, and colony formation of cancer cells. To investigate the role of ZWINT in proliferation, migration, invasion of cervical cancer, and evaluate the potential ability of ZWINT as a therapeutic target. First, ZWINT expression in cervical cancer was analyzed using the bioinformatic methods and assessed in several cervical cancer cell lines. The cell viability and colony formation assays were used to evaluate cell proliferation. Then, transwell assay was performed to investigate cell migration and invasion. Moreover, western blot was used to measure the expression level of ZWINT, matrix metalloproteinase 9 (MMP-9), N-cadherin, E-cadherin, p53 and p21 in CaSki and HeLa cells with ZWINT overexpression or knockdown. The bioinformatic analysis and western blot assay revealed the expression of ZWINT was significantly increased in cervical cancer. The cell viability and colony formation analysis illustrated that cell proliferation could be promoted by ZWINT overexpression and suppressed by ZWINT knockdown. Moreover, ZWINT promoted migration and invasion of CaSki and HeLa cells, through regulating the expression of MMP-9, N-cadherin, and E-cadherin. Furthermore, ZWINT attenuated the expression of p53 and p21 in cervical cancer cells. In summary, ZWINT functions in promoting cell proliferation, migration, and invasion of cervical cancer cells by suppressing p53/p21 signaling pathway, which indicated ZWINT is a potential therapeutic target for cervical cancer treatment.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70707523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Paricalcitol improved cardiac hypertrophy and fibrosis through upregulation of fibroblast growth factor-23 and downregulation of transforming growth factor-beta in a rat model of isoproterenol-induced cardiomyopathy.","authors":"Chieh-Jen Wu,&nbsp;Yu-He Li,&nbsp;Hsin-Hung Chen","doi":"10.4103/cjop.CJOP-D-23-00048","DOIUrl":"https://doi.org/10.4103/cjop.CJOP-D-23-00048","url":null,"abstract":"<p><p>Acute cardiomyopathy is a significant global health concern and one of the leading causes of death in developed countries. Prior studies have shown an association between acute cardiomyopathy and low vitamin D levels. Although paricalcitol, a vitamin D receptor (VDR) activator, has demonstrated clinical benefits in patients with advanced kidney disease, its effect on cardiac remodeling in cardiomyopathy is unknown. This study aimed to investigate the relative effects of paricalcitol on cardiomyopathy in rats. Wistar-Kyoto rats were administered vehicle (sham control group) or isoproterenol to induce cardiomyopathy. Rats administered isoproterenol were subsequently treated with paricalcitol (experimental group) or vehicle (isoproterenol group). Picrosirius red and immunofluorescence staining were used to analyze cardiac fibrosis and hypertrophy. Immunohistochemistry staining was used to confirm the molecular mechanisms involved in isoproterenol-induced cardiomyopathy in rats. Injection of paricalcitol could reduce collagen and transforming growth factor-beta 1 (TGF-β1) levels while activating fibroblast growth factor receptor 1 (FGFR1) and fibroblast growth factor-23 (FGF23) without the help of Klotho, thereby reducing myocardial hypertrophy and fibrosis. As a VDR activator, paricalcitol reduces isoproterenol-induced cardiac fibrosis and hypertrophy by reducing the expression of TGF-β1 and enhancing the expression of VDR, FGFR1, and FGF23.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71478668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA VPS9D1-AS1 regulates miR-187-3p/fibroblast growth factor receptor-like 1 axis to promote proliferation, migration, and invasion of prostate cancer cells.","authors":"Chenguang Wu,&nbsp;Jian Chen,&nbsp;Dong Wang","doi":"10.4103/cjop.CJOP-D-23-00054","DOIUrl":"https://doi.org/10.4103/cjop.CJOP-D-23-00054","url":null,"abstract":"<p><p>The morbidity and mortality of prostate cancer are increasing year by year, and the survival rate of prostate cancer patients after treatment is low. Therefore, investigating the molecular mechanism underlying prostate cancer is crucial for developing effective treatments. Recent studies have shown the important role of long-chain non-coding RNAs (lncRNAs) in tumorigenesis. VPS9D1-AS1 can modulate the progression of multiple cancers, but its molecular action mechanism in prostate cancer remains unknown. This study, therefore, intended to investigate the regulatory mechanism of VPS9D1-AS1 in prostate cancer. First, differentially expressed lncRNAs in prostate cancer were identified through bioinformatics approaches. The target lncRNA for the study was determined by reviewing the relevant literature and its downstream miRNA/mRNA axis was uncovered. Then, quantitative reverse transcription polymerase chain reaction was introduced to assess the expression of VPS9D1-AS1, miR-187-3p, and fibroblast growth factor receptor-like 1 (FGFRL1) at a cellular level, and Western blot was conducted to assess the protein level of FGFRL1 in cells. The results indicated that VPS9D1-AS1 and FGFRL1 were highly expressed in prostate cancer while miR-187-3p was less expressed. Besides, MTT, colony formation, wound healing, and cell invasion assays showed that silencing VPS9D1-AS1 inhibited the viability, migration ability, and invasion ability of prostate cancer cells. Dual-luciferase assay and RNA binding protein immunoprecipitation assay were performed to explore the interplay of miR-187-3p and VPS9D1-AS1 or FGFRL1. The results showed that VPS9D1-AS1 could sponge miR-187-3p, and FGFRL1 could serve as a direct target of miR-187-3p. Moreover, combined with the results of the rescue experiment, VPS9D1-AS1 was found to upregulate FGFRL1 by competitively sponging miR-187-3p to accelerate the malignant behaviors of prostate cancer cells. In conclusion, VPS9D1-AS1 could promote the phenotype progression of prostate cancer cells through targeting the miR-187-3p/FGFRL1 axis, and it has the potential to be a target for prostate cancer patients.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71478667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Asymmetry in sensory-motor function between the lower limbs in children with hemiplegic cerebral palsy: An observational study.","authors":"Hsiu-Ching Chiu,&nbsp;Louise Ada,&nbsp;Rong-Ju Cherng,&nbsp;Chiehfeng Chen","doi":"10.4103/cjop.CJOP-D-23-00057","DOIUrl":"https://doi.org/10.4103/cjop.CJOP-D-23-00057","url":null,"abstract":"<p><p>The objective of this study was to examine the difference in sensory-motor impairments (i.e., balance, contracture, coordination, strength, spasticity, and sensation) between legs in children with hemiplegic cerebral palsy. An observational study measured both lower limbs of children with hemiplegic cerebral palsy over one session. Six sensory-motor impairments (balance, coordination, strength, spasticity, contracture, and proprioception) were measured. The between-leg differences were analyzed using the paired t-tests and presented as the mean differences (95% confidence interval (CI)). Twenty-four participants aged 10.3 years (standard deviation: 1.3) participated. The affected leg was less than the less-affected leg in terms of the strength of dorsiflexors (mean difference (MD) -2.8 Nm, 95% CI -4.2 to -1.4), plantarflexors (MD -2.6 Nm, 95% CI -4.1 to -1.0), knee extensors (MD -5.3 Nm, 95% CI -10.2 to -0.5) as well as range of ankle dorsiflexion (MD -8 deg, 95% CI -13 to -3), and balance (median difference -11.1, 95% CI -11.6 to -10.6). There was a trend toward a difference in terms of the strength of hip abductors (MD -2.6 Nm, 95% CI -5.3 to 0.1) and coordination (MD -0.20 taps/s, 95% CI -0.42 to 0.01). The legs were similar in terms of the strength of hip extensors (MD 0.3 Nm, 95% CI -4.7 to 5.3), proprioception (MD 1 deg, 95% CI 0 to 2), and spasticity (median difference 0, 95% CI 0 to 0). Examination of the difference in sensory-motor impairments between legs in children with hemiplegic cerebral palsy has given us some insights into the deficits in both legs. Not only was balance, strength, and coordination decreased compared with the less-affected leg but also the less-affected leg was markedly decreased compared with typically developing children. Therefore, an intervention aimed at increasing muscle strength and coordination in both legs might have a positive effect, particularly on more challenging physical activities. This may, in turn, lead to successful participation in mainstream sport and recreation.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71478664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-22-3p ameliorates the symptoms of premature ovarian failure in mice by inhibiting CMKLR1 expression.","authors":"Miaomiao Pan","doi":"10.4103/cjop.CJOP-D-23-00004","DOIUrl":"10.4103/cjop.CJOP-D-23-00004","url":null,"abstract":"<p><p>Premature ovarian failure (POF) affects many adult women less than 40 years of age and leads to infertility. This study was aimed at exploring the improving effects of miR-22-3p on the symptoms of POF in mice by inhibiting chemokine-like receptor 1 (CMKLR1) expression. Female mice were intraperitoneally injected with cyclophosphamide to construct POF mice models. Lentiviral vectors containing miR-22-3p, short hairpin RNA (sh)-CMKLR1, and overexpression (oe)-CMKLR1, respectively, or in combination, were injected into the ovaries of both sides of POF mice. miR-22-3p and CMKLR1 expression in ovarian tissues of mice was assessed, and the targeting relationship between miR-22-3p and CMKLR1 was predicted and verified. Serum estradiol (E2), anti-Mullerian hormone, and follicle-stimulating hormone levels were assessed. Ovarian weight was weighed, and pathological changes and the number of primordial follicles, primary follicles, secondary follicles, and atresia follicles were observed. Apoptosis of ovarian tissues was determined. In ovarian tissues of POF mice, miR-22-3p expression was decreased while CMKLR1 expression was increased. miR-22-3p up-regulation or CMKLR1 down-regulation restored sex hormone levels, improved ovarian weight and the number of primordial follicles, primary follicles, and secondary follicles, and reduced the number of atresia follicle and ovarian granulosa cell apoptosis in POF mice. miR-22-3p targeted CMKLR1, and overexpressing CMKLR1 reversed the ameliorative effects of miR-22-3p overexpression on POF mice. Our research highlights that overexpressed miR-22-3p down-regulates CMKLR1 to ameliorate the symptoms of POF in mice. Therefore, the miR-22-3p/CMKLR1 axis could improve the symptoms of POF.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10459229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of neurotrophin receptor-interacting melanoma-associated antigen homolog inhibits acute myeloid leukemia cell growth via the ERK pathway.","authors":"Hongxia Zhang,&nbsp;Guangsheng Wu,&nbsp;Beili Chen","doi":"10.4103/cjop.CJOP-D-22-00162","DOIUrl":"10.4103/cjop.CJOP-D-22-00162","url":null,"abstract":"<p><p>Neurotrophin receptor-interacting melanoma-associated antigen homolog (NRAGE), a type II melanoma-associated antigen, plays a critical role in cell processes that are involved in the tumorigenesis of various cancers. However, the effect of NRAGE on acute myeloid leukemia (AML) is rarely reported. The expression of NRAGE in AML tissues and the survival rates between different AML groups were obtained from the GEPIA tool. Human AML cell lines were cultured and transfected with siRNA targeting NRAGE. The ability of AML cells to proliferate and cell cycle were examined. Western blotting was performed to detect the activity of the extracellular signal-regulated kinase (ERK) signaling pathway in AML cells. NRAGE expression was enhanced in AML tissues relative to control tissues, and the high NRAGE expression in AML patients is associated with a poor prognosis. The capacity of AML cells to survive and proliferate was significantly decreased and its cell cycle was arrested at the G1 phase after NRAGE was silenced. Furthermore, silencing NRAGE induced the inactivation of the ERK signaling pathway. Furthermore, supplement of tert-Butylhydroquinone, an ERK activator, improved the reduced ability of AML cell survival and proliferation as well as cell cycle arrest induced by NRAGE knockdown. In this study, NRAGE was identified as a tumor promoter in AML, which had an effect on cell proliferation, cell survival, and cell cycle through the ERK signaling pathway in AML cells.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10439695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Calycosin inhibits gemcitabine-resistant lung cancer cells proliferation through modulation of the LDOC1/GNL3L/NFκB.","authors":"Chi-Cheng Li,&nbsp;Cheng-You Lu,&nbsp;Chiung-Hung Hsu,&nbsp;Dennis Jine-Yuan Hsieh,&nbsp;Tso-Fu Wang,&nbsp;Tsung-Jung Ho,&nbsp;Wei-Wen Kuo,&nbsp;Cecilia Hsuan Day,&nbsp;Shih-Chieh Liao,&nbsp;Ming-Cheng Chen,&nbsp;Chih-Yang Huang","doi":"10.4103/cjop.CJOP-D-23-00009","DOIUrl":"10.4103/cjop.CJOP-D-23-00009","url":null,"abstract":"<p><p>Lung cancer is the most common malignant cancer worldwide. Combination therapies are urgently needed to increase patient survival. Calycosin is a phytoestrogen isoflavone that has been reported previously to inhibit tumor cell growth, although its effects on lung cancer remain unclear. The aim of this study was to investigate the effects of calycosin on cell proliferation and apoptosis of gemcitabine-resistant lung cancer cells. Using calycosin to treat human lung cancer cells (CL1-0) and gemcitabine-resistant lung cancer cells (CL1-0 GEMR) and examine the effects on the cells. Cultured human lung cancer cells (CL1-0) and gemcitabine-resistant lung cancer cells (CL1-0 GEMR) were treated with increasing concentrations of calycosin. Cell viability and apoptosis were studied by the 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide, flow cytometry, and TUNEL assays. Western blots were used to measure the expression levels of proliferation-related proteins and cancer stem cell proteins in CL1-0 GEMR cells. The results showed that calycosin treatment inhibited cell proliferation, decreased cell migration ability, and suppressed cancer stem cell properties in CL1-0 GEMR cells. Interestingly, in CL1-0 GEMR cells, calycosin treatment not only increased LDOC1 but also decreased GNL3L/NFκB protein levels and mRNA levels, in concentration-dependent manners. We speculate that calycosin inhibited cell proliferation of the gemcitabine-resistant cell line through regulating the LDOC1/GNL3L/NFκB pathway.</p>","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10459231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}