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MORPHOLOGICAL EVIDENCE FOR THE autocrine HYPOTHESIS

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Chinese Science Bulletin 1990年第24期35卷 2091-2093页

作者：刘明 Department of Thoracic Surgery China-Japan Friendship Hospital Beijing 100029 PRC

autocrine secretion is a concept which emerges in the search for the molecular basis of malignant tumour. Tumour cells can produce endogenous polypeptide growth factors which act on their producer cells via functional external receptors. This process has been termed 'autocrine secretion'. autocrine hypothesis explains the malignant growth of tumour cells satisfactorily. Transforming growth factor-α (TGF-α)is one of the typical autocrine growth factors. TGF-α can induce the reversible phenotypic transformation of normal rat kidney cells in the presence of other growth factors. This suggests that TGF-α may play an im-

关键词： autocrine bronchial carcinoma transforming growth factor-α electron microscope.

Gastrin as an autocrine growth factor in colorectal carcinoma:implications for therapy

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World Journal of Gastroenterology 1998年第6期4卷 6-8页

作者： Graham S. Baldwin and Arthur Shulkes

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关键词： autocrine loop colorectal neoplasms gastrin gastrin receptor progastrin

autocrine Production of Interleukin-6: A Mechanism of Interleukin-6 Independence in Dexamethasone-Resistant 7TD1 Murine Myeloma Cells

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Journal of Cancer Therapy 2014年第6期5卷 523-530页

作者： Kalyan J. Gangavarapu Alok Bhushan James C. K. Lai Christopher K. Daniels Department of Biomedical and Pharmaceutical Sciences College of Pharmacy The ISU Biomedical Research Institute Division of Health Sciences Idaho State University Pocatello USA Department of Pharmaceutical Sciences Jefferson School of Pharmacy Thomas Jefferson University Philadelphia USA

Several factors could contribute to proliferation of multiple myeloma (MM) cells independent of interleukin-6 (IL6) in the later stages of the disease. Our previous studies established a dexamethasone-resistant 7TD1 cell line (7TD1-Dxm) and have shown that one mechanism of resistance to dexamethasone is due to inhibition of cytochrome c release. We have also observed that 7TD1-Dxm cells proliferate independently of externally-added IL6. This study therefore aimed to elucidate the mechanisms responsible for IL6-independent proliferation in 7TD1-Dxm cells. Our results indicated that 7TD1-Dxm cells produced IL6 in an autocrine fashion. We have observed that dexamethasone-resistant 7TD1 cells become dexamethasone-resistant and IL6-independent for proliferation concomitantly. This strongly suggests that production of IL6 by 7TD1-Dxm cells may play an important role in the development of dexamethasone resistance. Consequently, further investigation of the molecular mechanisms responsible for IL6 production may be helpful in delineating the mechanisms leading to dexamethasone resistance.

关键词： Multiple Myeloma Interleukin-6 7TD1 Cells autocrine Production Dexamethasone Resistance

autocrine ACTIONS OF NADPH OXTOASE-DERIVED O2-IN CORONARY ARTERIAL MYOCYTES

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AUTOCRINE ACTIONS OF NADPH OXTOASE-DERIVED O2-IN CORONARY AR...

自体激泌素(autocrine)生长因子与癌

第十五届国际药理学大会

作者： Rachel W.Muh Department of Pharmacology and Toxicology Medical College of VirginiaVirginia Commonwealth UniversityRichmond VA 23298

＜正＞ The present study tested the hypothesis that extracellular O2. ? derived from NADPH oxidase （NOX） serves as an autocrine to activate physiological response in coronary arterial myocytes （CAMs）. By simultaneously monitoring intracellular（[O2.-]i） and extracellular O2.-([O2.-]o levels,M1 - receptor agonist oxotremorine （OXO） was found to stimulate a more rapid increase in [O2.-]O than [O2.-]i in CAMs. Addition of SOD outside cells blocked OXO- induced increases in both [O2.-]i and [O2.-]o. Silencing NOX subunit. Nox 1 by siRNAblocked increases in both [O2.-]i and [O2.-]o,but silencing Nox 4 only attenuated increase in [O2.-]*** ESR spectrometry. OXO was found to increase [O2.-]o by 35 %, which was blocked by Nox 1 siRNA （by 74%）. This Ml - activation of NOX stimulated SOD - blockable Ca2+ release in CAMs （△[Ca2+]i=821+++++67 nM）. NOX was also shown to be activated by NO donor, spermine NONOate （by 67 % ）. These results suggest that NOX - derived [O2.-]o exerts an autocrine action to stimulate intracellular Ca2+ release and that NOX can be activated by NO. which may counteract the action of excessive NO around CAMs.

关键词： NADPH oxidase autocrine redox signaling coronary artery

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国外医学.遗传学分册 1985年第6期 329-330页

作者：赵跃华

自体激泌素的分泌是恶性转化在分子水平以及细胞基础上提出的一种假说。在癌基因与肽类生长因子不同领域的研究中发现恶性肿瘤细胞的癌基因与自主性生长因子有关。恶性细胞内源性产生肽类生长因子作用于自己的受体,其表现型的表达过程... 详细信息

自体激泌素的分泌是恶性转化在分子水平以及细胞基础上提出的一种假说。在癌基因与肽类生长因子不同领域的研究中发现恶性肿瘤细胞的癌基因与自主性生长因子有关。恶性细胞内源性产生肽类生长因子作用于自己的受体,其表现型的表达过程称“自体激泌素的分泌”。自体激泌素假说的证据:在肿瘤细胞中,自体激泌素包括的生长因子有α型转化生长因子(TGFα)、与血小板生长因

关键词：生长因子癌基因受体肿瘤细胞 autocrine 自体

Endothelin increases the proliferation of rat olfactory mucosa cells

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Neural Regeneration Research 2020年第2期15卷 352-360页

作者： Bertrand Bryche Audrey Saint-Albin Claire Le Poupon Schlegel Christine Baly Patrice Congar Nicolas Meunier Neurobiologie de l'olfaction Institut National de Recherche Agronomique (INRA)Université Paris-SaclayJouy-en-JosasFrance Université de Versailles Saint-Quentin en Yvelines Département de BiologieVersaillesFrance

The olfactory mucosa holds olfactory sensory neurons directly in contact with an aggressive environment. In order to maintain its integrity, it is one of the few neural zones which are continuously renewed during the whole animal life. Among several factors regulating this renewal, endothelin acts as an anti-apoptotic factor in the rat olfactory epithelium. In the present study, we explored whether endothelin could also act as a proliferative factor. Using primary culture of the olfactory mucosa, we found that an early treatment with endothelin increased its growth. Consistently, a treatment with a mixture of BQ123 and BQ788(endothelin receptor antagonists) decreased the primary culture growth without affecting the cellular death level. We then used combined approaches of calcium imaging, reverse transcriptase-quantitative polymerase chain reaction and protein level measurements to show that endothelin was locally synthetized by the primary culture until it reached confluency. Furthermore, in vivo intranasal instillation of endothelin receptor antagonists led to a decrease of olfactory mucosa cell expressing proliferating cell nuclear antigen(PCNA), a marker of proliferation. Only short-term treatment reduced the PCNA level in the olfactory mucosa cells. When the treatment was prolonged, the PCNA level was not statistically affected but the expression level of endothelin was increased. Overall, our results show that endothelin plays a proliferative role in the olfactory mucosa and that its level is dynamically regulated. This study was approved by the Comité d’éthique en expérimentation animale COMETHEA(COMETHEA C2 EA-45;protocol approval #12-058) on November 28, 2012.

关键词： autocrine factor cell culture cellular dynamics endothelin olfaction olfactory basal cells olfactory epithelium olfactory mucosa primary culture

Redefining Human Vitamin D Sufficiency:Back to the Basics

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Bone Research 2013年第1期1卷 2-10页

作者： John S.Adams Jonathan Ramin Brandon Rafison Charles Windon Annika Windon Philip T.Liu Orthopaedic Hospital Research Center UCLA-Orthopaedic Hospital Department of Orthopaedic SurgeryDavid Geffen School of MedicineUCLA Department of Molecular Cell and Developmental BiologyDivision of Life SciencesCollege of Letters and ScienceUCLA

The role of the endocrine vitamin D pathway in regulating the serum calcium concentration in man is well described. In the presence of a low serum calcium level, the vitamin D metabolic pathway is called upon to produce more of the active vitamin D hormone, 1, 25-dihydroxyvitamin D （1, 25D）, via up-regulation of the CYP27b1-hydroxylase activity in the kidney. The consequence is mobilization of skeletal calcium stores to return the circulating calcium level back to the normal range. On the other hand, when the serum calcium level increases, endocrine forces move to suppress renal 1, 25D production and squelch bone resorption. It is now known that vitamin D metabolites also operate in an autocrine, paracrine and intracrine mode to control vitamin D receptor-directed biological responses at the tissue level. Because the metabolism and action of vitamin D occurs at the tissue level in this situation, use of circulating vitamin D metabolites and biomarkers to ascertain the local action of the vitamin D pathway is often misleading. This mini-review seeks to compare and contrast the operation of the vitamin D pathway at the endocrine and tissue level.

关键词： metabolism endocrine autocrine hormone biomarkers

Crosstalk between glioblastoma and tumor microenvironment drives proneural–mesenchymal transition through ligand-receptor interactions

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Genes & Diseases 2024年第2期11卷 874-889页

作者： Yancheng Lai Xiaole Lu Yankai Liao Pei Ouyang Hai Wang Xian Zhang Guanglong Huang Songtao Qi Yaomin Li Department of Neurosurgery Institute of Brain DiseaseNanfang HospitalSouthern Medical UniversityGuangzhouGuangdong 510515China Laboratory for Precision Neurosurgery Nanfang HospitalSouthern Medical UniversityGuangzhouGuangdong 510515China

Glioblastoma(GBM)is the most common intrinsic and aggressive primary brain tumor in adults,with a median survival of approximately 15 *** heterogeneity is considered responsible for the treatment resistance and unfavorable ***-mesenchymal transition(PMT)represents GBM malignant progression and recurrence,which might be a breakthrough to understand GBM heterogeneity and overcome treatment *** is a complicated process influenced by crosstalk between GBM and tumor microenvironment,depending on intricate ligand-receptor *** this review,we summarize the autocrine and paracrine pathways in the GBM microenvironment and related ligand-receptor interactions inducing *** also discuss the current therapies targeting the PMT-related autocrine and paracrine ***,this review offers a comprehensive understanding of the failure of GBM-targeted therapy and ideas for future tendencies of GBM treatment.

关键词： autocrine Glioblastoma Ligand-receptor interaction Microenvironment Paracrine Proneural-mesenchymal transition

Hepatopoietin Cn suppresses apoptosis of human hepatocellular carcinoma cells by up-regulating myeloid cell leukemia-1

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World Journal of Gastroenterology 2010年第2期16卷 193-200页

作者： Chu-Tse Wu Department of Experimental Hematology Beijing Institute of Radiation Medicine27 Taiping Road

AIM:To investigate the role of hepatopoietin Cn(HPPCn) in apoptosis of hepatocellular carcinoma(HCC)cells and its mechanism. METHODS:Two human HCC cell lines,SMMC7721 and HepG2,were used in this ***, Western blotting and enzyme linked immunosorbent assay were conducted to identify the expression of HPPCn and the existence of an autocrine loop of HPPCn/ HPPCn receptor in SMMC7721 and *** cells were detected using fluorescein isothiocyanate (FITC)-conjugated Annexin V and propidium ***:The HPPCn was highly expressed in human HCC cells and secreted into culture medium(CM). FITC-labeled recombinant human protein(rhHPPCn) could specifically bind to its receptor on HepaG2 cells. Treatment with 400 ng/mL rhHPPCn dramatically increased the viability of HCC-derived cells from 48.1% and 36.9%to 85.6%and 88.4%,respectively(P< 0.05).HPPCn silenced by small-interfering RNA reduced the expression and secretion of HPPCn and increased the apoptosis induced by trichostatin ***, HPPCn could up-regulate the expression of myeloid cell leukemia-1(Mcl-1)in HCC cells via mitogen-activated protein kinase(MAPK)and sphingosine kinase-1. CONCLUSION:HPPCn is a novel hepatic growth factor that can be secreted to CM and suppresses apoptosis of HCC cells by up-regulating Mcl-1 expression.

关键词： Hepatopoietin Cn autocrine Hepatocellular carcinoma Apoptosis Myeloid cell leukemia-1