Growth factorsPub Date : 2022-11-01DOI: 10.1080/08977194.2022.2108809
Yan Zhang, Yuanyuan Duan, Chenguang Wu, Wen Peng, Wenyu Chen, Li Wang, Zhaoqun Deng
{"title":"MiR-200c regulates invasion, proliferation and EMT of anaplastic thyroid cancer cells by targeting parathyroid hormone like hormone.","authors":"Yan Zhang, Yuanyuan Duan, Chenguang Wu, Wen Peng, Wenyu Chen, Li Wang, Zhaoqun Deng","doi":"10.1080/08977194.2022.2108809","DOIUrl":"https://doi.org/10.1080/08977194.2022.2108809","url":null,"abstract":"<p><p>This study aimed to explore the specific effect of miR-200c in anaplastic thyroid cancer (ATC). Hth74 and ARO cell lines were used. Proliferation, invasion, and colony formation activities of Hth74 and ARO cell lines affected by miR-200c were studied. Expression of epithelial-to-mesenchymal transition (EMT) markers (E-cadherin, N-cadherin, Slug, and Snail) in the Hth74 and ARO cell lines were validated by western blot and qRT-PCR. In addition, the regulation of the parathyroid hormone-like hormone (PTHLH) by miR-200c was assessed. Overexpression of miR-200c inhibited the invasion, proliferation, and colony formation of the ATC cell lines, whereas its downregulation achieved the opposite results. PTHLH was found to be regulated negatively by miR-200c through a miR-200c binding site within the 3'-UTR of PTHLH. miR-200c repressed the proliferation, invasion, and EMT process of cells in ATC cell lines by targeting PTHLH post-transcriptionally, which indicates that miR-200c may be a potential target for the treatment of ATC.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10803226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Growth factorsPub Date : 2022-11-01DOI: 10.1080/08977194.2022.2124915
Katarina Mirjačić Martinović, Ana Vuletić, Emina Mališić, Tatjana Srdić-Rajić, Nevena Tišma Miletić, Nada Babović, Vladimir Jurišić
{"title":"Increased circulating TGF-β1 is associated with impairment in NK cell effector functions in metastatic melanoma patients.","authors":"Katarina Mirjačić Martinović, Ana Vuletić, Emina Mališić, Tatjana Srdić-Rajić, Nevena Tišma Miletić, Nada Babović, Vladimir Jurišić","doi":"10.1080/08977194.2022.2124915","DOIUrl":"https://doi.org/10.1080/08977194.2022.2124915","url":null,"abstract":"<p><p>Transforming growth factor beta (TGF-β) plays a complex role in carcinogenesis. In 30 melanoma patients and 20 healthy controls (HC) we analysed functional and phenotypic characteristics of NK cells by Flow cytometry, gene expression of TGF-β1 in peripheral blood mononuclear cells by qPCR and serum and supernatant level of free TGF-β1 by ELISA. Melanoma patients had significantly higher serum level of circulatingTGF-β1 compared to HC, especially those with metastasis into the central nervous system (subclass M1d) and high LDH serum values. Melanoma patients compared to HC had significantly higher level of <i>TGF-β1</i> gene in PBMC. TGF-β1 serum values negatively correlate with NK cell activity analysed by CD107a (degranulation marker), IFN-γ, NKG2D, and NKp46 in patients. Study shows the association of high level of TGF-β1 with NK cell inhibition in patients represents the main mechanism of tumour immune evasion. Targeting TGF-β may become an important cancer treatment for improving antitumor immunity.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9344848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Growth factorsPub Date : 2022-11-01DOI: 10.1080/08977194.2022.2109469
Ling Qiang Bai, Bin Zhe Wang, Qi Wei Liu, Wen Qiang Li, Hang Zhou, Xiao Yan Yang
{"title":"Effects of penehyclidine hydrochloride on myocardial ischaemia-reperfusion injury in rats by inhibiting TLR4/MyD88/NF-κB pathway via miR-199a-3p.","authors":"Ling Qiang Bai, Bin Zhe Wang, Qi Wei Liu, Wen Qiang Li, Hang Zhou, Xiao Yan Yang","doi":"10.1080/08977194.2022.2109469","DOIUrl":"https://doi.org/10.1080/08977194.2022.2109469","url":null,"abstract":"<p><p>This study was to probe the role of penehyclidine hydrochloride (PHC) mediating the impact of toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-κB) signalling pathway on myocardial ischaemia-reperfusion injury (MI/RI) in rats through miR-199a-3p. The rat MI/RI model was established through ligating left anterior descending (LAD) coronary artery. PHC was injected preoperatively into the model rats, and injected with miR-199a-3p lentiviral vector or TLR4 antagonist (TAK-242). Next, cardiac function of rats was examined by echocardiography, and rat serum indicators, oxidative stress levels and inflammatory factors were detected. HE staining was applied to detect pathological tissue structure, TUNEL staining to detect apoptosis rate, qRCR and western blot to detect miR-199a-3p and TLR4/MyD88/NF-κB expressions in rat myocardial tissues. Dual luciferase reporter experiment was conducted to confirm the relationship between miR-199a-3p and TLR4. In conclusion, PHC suppresses TLR4/MyD88/NF-κB signalling pathway through miR-199a-3p, thereby improving MI/RI in rats.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10797623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Growth factorsPub Date : 2022-11-01DOI: 10.1080/08977194.2022.2126317
Hussein Kadhem Al-Hakeim, Qasim Jasim Al-Kaabi, Michael Maes
{"title":"High mobility group box 1 and Dickkopf-related protein 1 as biomarkers of glucose toxicity, atherogenicity, and lower β cell function in patients with type 2 diabetes mellitus.","authors":"Hussein Kadhem Al-Hakeim, Qasim Jasim Al-Kaabi, Michael Maes","doi":"10.1080/08977194.2022.2126317","DOIUrl":"https://doi.org/10.1080/08977194.2022.2126317","url":null,"abstract":"<p><p>Type 2 diabetes mellitus (T2DM) is associated with increased atherogenicity and inflammatory responses, which may be related to high mobility group box 1 (HMGB1) and Dickkopf-related protein 1 (DKK1). The role of HMGB1 and DKK1 in T2DM is examined in association with lipid and insulin profiles. Serum HMGB1 and DKK1 were measured in T2DM with and without hypertension and compared with controls. The results showed that HMGB1 and DKK1 are higher in T2DM irrespective of hypertension. A large part of the variance in the β-cell index and glucose toxicity was explained by the combined effects of HMGB1 and DKK1. In conclusion, both HMGB1 and DKK1 may contribute to increased atherogenicity in T2DM. Moreover, both biomarkers may cause more deficits in β-cell function and increase glucose toxicity leading to the development of more inflammation and diabetic complications. HMGB1 and the Wnt pathways are other drug targets in treating T2DM.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10785957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Matrine induces hepatocellular carcinoma apoptosis and represses EMT and stemness through microRNA-299-3p/PGAM1 axis.","authors":"BaoLin Wang, HuiHai Wang, Qin Zhao, Fei Lu, ZhenZhuang Yan, Fang Zhou, QingLun Su","doi":"10.1080/08977194.2022.2113073","DOIUrl":"https://doi.org/10.1080/08977194.2022.2113073","url":null,"abstract":"<p><p>This study explored the impacts of matrine on hepatocellular carcinoma (HCC) cell growth, metastasis, epithelial-mesenchymal transition (EMT), and stemness through regulating the microRNA <i>(miR)-299-3p</i>/<i>phosphoglycerate mutase 1</i> (<i>PGAM1</i>) axis. The association between <i>miR-299-3p</i> expression with the prognosis of HCC patients was studied. <i>miR-299-3p</i> and <i>PGAM1</i> sequences were transfected into matrine-treated HCC cells, and cell proliferation, invasion, apoptosis, and stemness were detected, as well as protein expression of EMT- and stemness-related makers. The targeting relationship between <i>miR-299-3p</i> and <i>PGAM1</i> was identified. Matrine elevated <i>miR-299-3p</i> expression, repressed proliferation, invasion, and anti-apoptosis of HCC cells, and constrained EMT and stemness <i>in vitro</i>. <i>PGAM1</i> was a target of <i>miR-299-3p</i>. Repression of <i>PGAM1</i> rescued the effects of <i>miR-299-3p</i> downregulation on HCC cells. Matrine stimulates HCC cell apoptosis and represses the process of EMT and stemness through the <i>miR-299-3p</i>/<i>PGAM1</i> axis.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10793795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Growth factorsPub Date : 2022-11-01DOI: 10.1080/08977194.2022.2113394
Jing Lin, Xiaochun Wu
{"title":"Halofuginone inhibits cell proliferation and AKT/mTORC1 signaling in uterine leiomyoma cells.","authors":"Jing Lin, Xiaochun Wu","doi":"10.1080/08977194.2022.2113394","DOIUrl":"https://doi.org/10.1080/08977194.2022.2113394","url":null,"abstract":"<p><p>The present study aimed to explore the effects of antifibrotic agent halofuginone on uterine leiomyomas (ULs) cells. The survival of the uterine smooth muscle (UtSMC) cells and UL ELT3 cells were measured. Flow cytometry was used to assess the cell cycle distribution and apoptosis. Effects of halofuginone on the state of AKT/mTOR pathway were evaluated. Xenograft animal model was applied to explore the effects of halofuginone <i>in vivo</i>. Halofuginone inhibited the proliferation of ELT3 cells dose-dependently without obvious influence on UtSMC cells. Halofuginone suppressed cell cycle progression and promoted apoptosis of ELT3 cells dose-dependently. Also, p-AKT/AKT and p-p70S6/p70S6 were significantly lowered after treatment with 20 nM halofuginone. Additionally, halofuginone reduced ELT3 tumor growth in xenograft tumor animal model. The present study illustrates that halofuginone inhibits cell proliferation of ULs with low side effects on normal smooth muscle cells, and AKT/mTOR signaling pathway was inactivated meanwhile.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10796660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Embryonic growth retardation and altered expression of IGF-II is reciprocal induced by phytocompounds during early gestation in mice.","authors":"Khamhee Wangsa, Krishnakshi Misra, Upasa Gowala, Indira Sarma, Purba Jyoti Saikia, Hirendra Nath Sarma","doi":"10.1080/08977194.2022.2129018","DOIUrl":"https://doi.org/10.1080/08977194.2022.2129018","url":null,"abstract":"<p><p>Methanolic crude extract of <i>Scoparia dulcis</i> (CESD) was orally administered to female mice during the early gestation (day 4-day 8) at a dose of 500<b> </b>mg/kg/day. It induces embryo resorption and morphological changes of fetal maternal tissue. Histomorphology was studied by routine hematoxylin eosin stain. In situ immunofluorescence localization of IGF-II using Texas red showed an ordered expression of the growth factor in the maternal decidual cells, trophoblast cells and the embryo. Western blot analysis showed a gradual increase of IGF-II from D4 to D8 of control females. In contrast, the CESD-treated females showed resorption of embryo on D8 with disorganized in situ expression and lowered IGF-II in fetal maternal tissue. The phytocompounds present in the CESD could modulate either the ER or IGF-II receptors causing reduced IGF-II expression in the target tissues which lead to the failure of embryonic growth during periimplantation.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10785965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Growth factorsPub Date : 2022-11-01DOI: 10.1080/08977194.2022.2118119
Lingli Guo, Baohua Wei, Feng Pan, Hasi Wulan, Mi Cai
{"title":"Effects of dual-gene modification on biological characteristics of vascular endothelial cells and their significance as reserving cells for chronic wound repair.","authors":"Lingli Guo, Baohua Wei, Feng Pan, Hasi Wulan, Mi Cai","doi":"10.1080/08977194.2022.2118119","DOIUrl":"https://doi.org/10.1080/08977194.2022.2118119","url":null,"abstract":"<p><p>bFGF is a commonly used and reliable factor for improving chronic wound healing, and hSulf-1 expression is abundant in surrounding cells of chronic wound tissue and vascular endothelial cells, which can reverse the effect of bFGF and inhibit the signalling activity of cell proliferation. In this study, an adenovirus, Ad5F35ET1-bFGF-shSulf1, was designed for establishing the dual-gene modified vascular endothelial cells, which were used as the repair cells for skin chronic wound. Ad5F35ET1-bFGF-shSulf1 infected ECV304 cells in vitro and mediated the overexpression of bFGF and the knockdown of hSulf-1, which effectively activated the AKT and ERK signal transduction pathways, facilitate cell proliferation and migration, with the cell viability to 128.29% at 72 h after infection, compared to 66.65%, 73.74%, 87.63%, 103.14% in the blank control, Ad5F35ET1-EGFP-shNC, Ad5F35ET1-shSulf1, Ad5F35ET1-bFGF groups, respectively. In the rat ear skin injury model, the wound healing was significantly accelerated in the Ad5F35ET1-rbFGF-shrSulf1 group compared to the blank control group (<i>p</i> = 0.0046), Ad5F35ET1-EGFP-shNC group (<i>p</i> = 0.0245), Ad5F35ET1-shrSulf group (<i>p</i> = 0.0426), and Ad5F35ET1-rbFGF group (<i>p</i> = 0.2853). The results demonstrated that this strategy may be a candidate therapy for chronic injury repair.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10798112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The expression of BMP, integrin, ZEB2 in ovarian high-grade serous carcinoma in relation with lymph node metastasis.","authors":"Elham Bahador Zırh, Elif Taşar Kapaklı, Anıl Dolgun, Alp Usubütün, Naciye Dilara Zeybek","doi":"10.1080/08977194.2022.2099849","DOIUrl":"https://doi.org/10.1080/08977194.2022.2099849","url":null,"abstract":"<p><p>Ovarian cancer (OC) is clinically important because it is diagnosed late and has metastasis when it is diagnosed. Mortality risk increases 2.75 times in the presence of lymph node (LN) metastasis. During metastasis, many molecules including BMPs originated from stroma, and tumor cells participate through transcription factors and integrins for cytoskeleton regulation during cell migration. We hypothesized an inverse correlation between BMP2 and BMP7 along with changes in ZEB2, and integrin α5β1 in high-grade OCs in relation to LN metastasis. The BMP2 immunoreactivity was strong along with strong ZEB2 and weak integrins' immunoreactivity in samples with LN metastasis. Strong immunoreactivity of BMP7 was accompanied by strong immunoreactivity of integrins in the samples without LN metastasis. Study results showed BMP2's strong positive immunoreactivity and weak BMP7 immunoreactivity in tumor cells with a significantly weak inverse correlation. This inverse correlation should be considered as both BMPs have different effects in the window of cancer progression and invasion.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40530970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Growth factorsPub Date : 2022-08-01Epub Date: 2022-07-21DOI: 10.1080/08977194.2022.2087520
Oliver Cucanic, Rae H Farnsworth, Steven A Stacker
{"title":"The cellular and molecular mediators of metastasis to the lung.","authors":"Oliver Cucanic, Rae H Farnsworth, Steven A Stacker","doi":"10.1080/08977194.2022.2087520","DOIUrl":"https://doi.org/10.1080/08977194.2022.2087520","url":null,"abstract":"<p><p>Organ-specific metastasis to secondary organs is dependent on the formation of a supportive pre-metastatic niche. This tissue-specific microenvironmental response is thought to be mediated by mutational and epigenetic changes to primary tumour cells resulting in altered cross-talk between cell types. This response is augmented through the release of tumour and stromal signalling mediators including cytokines, chemokines, exosomes and growth factors. Although researchers have elucidated some of the cancer-promoting features that are bespoke to organotropic metastasis to the lungs, it remains unclear if these are organ-specific or generic between organs. Understanding the mechanisms that mediate the metastasis-promoting synergy between the host microenvironment, immunity, and pulmonary structures may elucidate predictive, prognostic and therapeutic markers that could be targeted to reduce the metastatic burden of disease. Herein, we give an updated summary of the known cellular and molecular mechanisms that contribute to the formation of the lung pre-metastatic niche and tissue-specific metastasis.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40634297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}