Steroid-induced cell proliferation in vivo is associated with increased c-myc proto-oncogene transcript abundance

Development ◽  
1988 ◽  
Vol 104 (1) ◽  
pp. 87-95
Author(s):  
S.A. Rempel ◽  
R.N. Johnston
Keyword(s):  
Cell Proliferation ◽  
Growth Factors ◽  
Steroid Hormones ◽  
Steroid Hormone ◽  
Normal Liver ◽  
Transcript Abundance ◽  
Chicken Oviduct ◽  
Massive Cell ◽  
In Cells

Enhanced c-myc transcript abundance has been observed in a variety of human malignancies, in normal liver tissue induced to proliferate in vivo by partial hepatectomy and in cells in culture induced to proliferate with the addition of protein hormones and growth factors. Little is known, however, about the expression of cellular proto-oncogenes in cells induced to proliferate in vivo by steroid hormones. Experiments reported here indicate that when cells of the immature chicken oviduct are induced to undergo rapid in vivo proliferation by application of the estrogen hormone 17 beta-estradiol, the onset of this proliferation is associated with a rapid, large, and transient increase in c-myc transcript abundance. When estrogen is administered to chickens in which the oviduct has already differentiated, neither massive cell proliferation nor large increases in c-myc transcript abundance are induced. We conclude that the abundance of c-myc transcripts in vivo correlates well with the degree of cell proliferation induced by steroid hormone.

scholarly journals Anti-Angiogenic Treatments Interact with Steroid Secretion in Inflammatory Breast Cancer Triple Negative Cell Lines

Cancers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 3668
Author(s):  
Ángela Alonso-Diez ◽  
Sara Cáceres ◽  
Laura Peña ◽  
Belén Crespo ◽  
Juan Carlos Illera
Keyword(s):  
Breast Cancer ◽  
Growth Factors ◽  
Steroid Hormones ◽  
Cell Lines ◽  
Inflammatory Breast Cancer ◽  
Steroid Hormone ◽  
Sex Steroid ◽  
Antiangiogenic Therapies

Human inflammatory breast cancer (IBC) is a highly angiogenic disease for which antiangiogenic therapy has demonstrated only a modest response, and the reason for this remains unknown. Thus, the purpose of this study was to determine the influence of different antiangiogenic therapies on in vitro and in vivo steroid hormone and angiogenic growth factor production using canine and human inflammatory breast carcinoma cell lines as well as the possible involvement of sex steroid hormones in angiogenesis. IPC-366 and SUM149 cell lines and xenotransplanted mice were treated with different concentrations of VEGF, SU5416, bevacizumab and celecoxib. Steroid hormone (progesterone, dehydroepiandrostenedione, androstenedione, testosterone, dihydrotestosterone, estrone sulphate and 17β-oestradiol), angiogenic growth factors (VEGF-A, VEGF-C and VEGF-D) and IL-8 determinations in culture media, tumour homogenate and serum samples were assayed by EIA. In vitro, progesterone- and 17β-oestradiol-induced VEGF production promoting cell proliferation and androgens are involved in the formation of vascular-like structures. In vivo, intratumoural testosterone concentrations were augmented and possibly associated with decreased metastatic rates, whereas elevated E1SO4 concentrations could promote tumour progression after antiangiogenic therapies. In conclusion, sex steroid hormones could regulate the production of angiogenic factors. The intratumoural measurement of sex steroids and growth factors may be useful to develop preventive and individualized therapeutic strategies.

TeBG- and CBG-bound steroid hormones in rabbits are available for influx into uterus in vivo

1988 ◽  
Vol 254 (1) ◽  
pp. E79-E83
Author(s):  
G. Chaudhuri ◽  
K. A. Steingold ◽  
W. M. Pardridge ◽  
H. L. Judd
Keyword(s):  
Steroid Hormones ◽  
Plasma Proteins ◽  
Steroid Hormone ◽  
Rabbit Serum ◽  
Injection Technique ◽  
Metabolic Clearance ◽  
Adrenal Steroid ◽  
Corticosteroid Binding Globulin

The metabolic clearance rate (MCR) of gonadal or adrenal steroid hormones in rabbits often does not bear the expected inverse relationship with hormone binding to testosterone-binding globulin (TeBG) or corticosteroid-binding globulin (CBG). This suggests TeBG or CBG may not impede steroid hormone delivery to tissues. The effects of rabbit plasma proteins on the influxes of 3H-labeled steroids from the circulation into the rabbit uterus were measured in vivo using a tissue sampling single-injection technique. In the absence of plasma proteins, estradiol (E2) and testosterone (T) were freely diffusible through the uterine microvasculature (i.e., extraction greater than 80%). The extractions of dihydrotestosterone (DHT) and corticosterone (B) ranged from 60 to 72%, while that of cortisol (F) was reduced at 40%. Rabbit serum exerted no inhibition of the influxes of the steroids tested. The influxes of T and B greatly exceeded the rates that would be expected if only the free and albumin-bound fractions estimated in vitro were diffusible in vivo. However, the extraction of [3H]corticosteroid-binding globulin or bovine [3H]albumin were low, consistent with little, if any, extravascular uptake of the plasma proteins. The results indicate both albumin-bound and globulin-bound steroid hormone are available for transport into the uterus in the rabbit in vivo without significant exodus of the plasma protein, per se.

scholarly journals PTP4A3, A Novel Target Gene of HIF-1alpha, Participates in Benzene-Induced Cell Proliferation Inhibition and Apoptosis through PI3K/AKT Pathway

2020 ◽  
Vol 17 (3) ◽  
pp. 910
Author(s):  
Yunqiu Pu ◽  
Fengxia Sun ◽  
Rongli Sun ◽  
Zhaodi Man ◽  
Shuangbin Ji ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Target Gene ◽  
Akt Pathway ◽  
Proliferation Inhibition ◽  
Cell Proliferation Inhibition ◽  
A Cell ◽  
Novel Target ◽  
In Cells

Benzene, a commonly used chemical, has been confirmed to specifically affect the hematopoietic system as well as overall human health. PTP4A3 is overexpressed in leukemia cells and is related to cell proliferation. We previously found that HIF-1alpha was involved in benzene toxicity and PTP4A3 may be the target gene of HIF-1alpha via ChIP-seq. The aim of this study is to confirm the relationship between HIF-1alpha and PTP4A3 in benzene toxicity, as well as the function of PTP4A3 on cell toxicity induced by 1,4-benzoquinone (1,4-BQ). Our results indicate that HIF-1alpha could regulate PTP4A3 with in vivo and in vitro experiments. A cell line with suppressed PTP4A3 was established to investigate the function of PTP4A3 in 1,4-BQ toxicity in vitro. The results revealed that cell proliferation inhibition was more aggravated in PTP4A3 low-expression cells than in the control cells after 1,4-BQ treatment. The relative oxygen species (ROS) significantly increased in cells with inhibited PTP4A3, while the rise was inferior to the control cells at the 20 μM 1,4-BQ group. An increase in DNA damage was seen in PTP4A3 down-regulated cells at the 10 μM 1,4-BQ group, whereas the results reversed at the concentration of 20 μM. Moreover, the apoptosis rate increased higher in down-regulated PTP4A3 cells after 1,4-BQ exposure. In addition, PI3K/AKT pathway was significantly restrained in cells with inhibited PTP4A3 after 1,4-BQ treatment. Our results indicate that HIF-1alpha may regulate PTP4A3 to be involved in benzene toxicity. Inhibition of PTP4A3 could aggravate cell proliferation suppression and apoptosis by regulating PI3K/AKT pathway after 1,4-BQ treatment.

scholarly journals Blocking Wnt signaling by SFRP-like molecules inhibits in vivo cell proliferation and tumor growth in cells carrying active β-catenin

Oncogene ◽  
2010 ◽  
Vol 30 (4) ◽  
pp. 423-433 ◽  
Author(s):  
E Lavergne ◽  
I Hendaoui ◽  
C Coulouarn ◽  
C Ribault ◽  
J Leseur ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Growth ◽  
Wnt Signaling ◽  
In Cells

In-vitro production and pre-validation of lyophilized canine platelet-rich plasma for therapeutic use

2021 ◽  
Vol 41 ◽  
Author(s):  
Natália P.P. Freitas ◽  
Maria Márcia M.S. Maior ◽  
Beatriz A.P. Silva ◽  
Marcus R.L. Bezerra ◽  
José F. Nunes ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Cell Proliferation ◽  
Growth Factors ◽  
Platelet Rich Plasma ◽  
Three Dimensional ◽  
In Vitro Production ◽  
Mesh Structure ◽  
Prp Gel

ABSTRACT: Platelet-rich plasma (PRP) has been considered a promising therapeutic alternative, since platelets are rich in growth factors that are used in the Regenerative Medicine field. However, fresh PRP cannot be stored for long periods. This study aimed to develop a protocol for obtaining lyophilized canine PRP capable of maintaining viability after its reconstitution. For that purpose, canine PRP extraction and lyophilization protocols were initially tested. Subsequently, assays were carried out to quantify the growth factors VEGF and TGF-β, before and after the lyophilization process, gelation test and the three-dimensional gel structure analysis of the reconstituted lyophilized PRP by electron microscopy, as well as in vitro cell proliferation test in lyophilized PRP gel. Additionally, the immunogenicity test was performed, using allogeneic samples of lyophilized PRP. The results showed that the lyophilized PRP had adequate therapeutic concentrations of growth factors VEGF and TGF-β (9.1pg/mL and 6161.6pg/mL, respectively). The reconstituted PRP gel after lyophilization showed an in vitro durability of 10 days. Its electron microscopy structure was similar to that of fresh PRP. In the cell proliferation test, an intense division process was verified in mesenchymal stem cells (MSCs) through the three-dimensional mesh structure of the lyophilized PRP gel. The immunogenicity test showed no evidence of an immune reaction. The findings were promising, suggesting the possibility of having a lyophilized canine PRP that can be marketed. New in vivo and in vitro studies must be carried out for therapeutic confirmation.

scholarly journals Epidermal and fibroblast growth factors incorporated polyvinyl alcohol electrospun nanofibers as biological dressing scaffold

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Amnah Asiri ◽  
Syafiqah Saidin ◽  
Mohd Helmi Sani ◽  
Rania Hussien Al-Ashwal
Keyword(s):  
Cell Proliferation ◽  
Growth Factors ◽  
Growth Factor ◽  
Polyvinyl Alcohol ◽  
Wound Dressing ◽  
Electrospun Nanofibers ◽  
In Vivo Studies ◽  
Fibroblast Growth ◽  
Biological Dressing

AbstractIn this study, single, mix, multilayer Polyvinyl alcohol (PVA) electrospun nanofibers with epidermal growth factor (EGF) and fibroblast growth factor (FGF) were fabricated and characterized as a biological wound dressing scaffolds. The biological activities of the synthesized scaffolds have been verified by in vitro and in vivo studies. The chemical composition finding showed that the identified functional units within the produced nanofibers (O–H and N–H bonds) are attributed to both growth factors (GFs) in the PVA nanofiber membranes. Electrospun nanofibers' morphological features showed long protrusion and smooth morphology without beads and sprayed with an average range of 198–286 nm fiber diameter. The fiber diameters decrement and the improvement in wettability and surface roughness were recorded after GFs incorporated within the PVA Nanofibers, which indicated potential good adoption as biological dressing scaffolds due to the identified mechanical properties (Young’s modulus) in between 18 and 20 MPa. The MTT assay indicated that the growth factor release from the PVA nanofibers has stimulated cell proliferation and promoted cell viability. In the cell attachment study, the GFs incorporated PVA nanofibers stimulated cell proliferation and adhered better than the PVA control sample and presented no cytotoxic effect. The in vivo studies showed that compared to the control and single PVA-GFs nanofiber, the mix and multilayer scaffolds gave a much more wound reduction at day 7 with better wound repair at day 14–21, which indicated to enhancing tissue regeneration, thus, could be a projected as a suitable burn wound dressing scaffold.

Characteristics of steroid hormone receptors in cultured MC3T3-E1 osteoblastic cells and effect of steroid hormones on cell proliferation

1992 ◽  
Vol 51 (5) ◽  
pp. 376-381 ◽  
Author(s):  
Akihiro Masuyama ◽  
Yasuyoshi Ouchi ◽  
Fumiyasu Sato ◽  
Takyauki Hosoi ◽  
Tetsuro Nakamura ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Steroid Hormones ◽  
Hormone Receptors ◽  
Steroid Hormone ◽  
Steroid Hormone Receptors ◽  
Osteoblastic Cells

scholarly journals PYCR1 interference inhibits cell growth and survival via c-Jun N-terminal kinase/insulin receptor substrate 1 (JNK/IRS1) pathway in hepatocellular cancer

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Juhua Zhuang ◽  
Yanan Song ◽  
Ying Ye ◽  
Saifei He ◽  
Xing Ma ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Tumor Growth ◽  
Insulin Receptor ◽  
Cell Apoptosis ◽  
Normal Liver ◽  
Insulin Receptor Substrate ◽  
Growth And Survival ◽  
Qrt Pcr

Abstract Background Liver cancer is the second leading causes of cancer-related death globally. Pyrroline-5-carboxylate reductase 1 (PYCR1) plays a critical role in metabolic profiles of tumors. Therefore, it is necessary to explore the mechanisms of PYCR1 on cell growth and survival in hepatocellular carcinoma (HCC). Methods Protein and mRNA expression levels of PYCR1 in 140 pairs of tumor and adjacent normal liver tissues of HCC patients were analyzed by immunohistochemistry and quantitative real-time polymerase chain reaction (qRT-PCR). Expressions of PYCR1 were inhibited in BEL-7404 cells and SMMC-7721 cells using gene interference technology. The cell proliferation was detected by Celigo and MTT assay. The colony formation assay was also performed. The cell apoptosis was measured by flow cytometric assay. The effect of PYCR1 interference on tumor growth was observed by xenograft nude mice assay in vivo. The downstream pathway of PYCR1 interference was searched by microarray and bioinformatics analysis, and validated by qRT-PCR and western blot. Results PYCR1 levels were significantly up-regulated in HCC tumor tissues than adjacent normal liver tissues in both protein and mRNA levels (P < 0.01). In vitro, the cell proliferation was significantly slower in shPYCR1 group than shCtrl group in BEL-7404 and SMMC-7721 cells (P < 0.001). The colony number was significantly smaller after PYCR1 interference (P < 0.01). The percentage of apoptosis cells significantly increased in shPYCR1 group (P < 0.01). In vivo, PYCR1 interference could obviously suppress tumor growth in xenograft nude mice. The volume and weight of tumors were significantly smaller via PYCR1 interference. The c-Jun N-terminal kinase (JNK) signaling pathway significantly altered, and insulin receptor substrate 1 (IRS1) were significantly down-regulated by PYCR1 interference in both mRNA and protein levels (P < 0.001). Conclusion PYCR1 interference could inhibit cell proliferation and promote cell apoptosis in HCC through regluting JNK/IRS1 pathway. Our study will provide a drug target for HCC therapy and a potential biomarker for its diagnosis or prognosis.

scholarly journals Salt-inducible kinase inhibition suppresses acute myeloid leukemia progression in vivo

Blood ◽  
2020 ◽  
Vol 135 (1) ◽  
pp. 56-70 ◽  
Author(s):  
Yusuke Tarumoto ◽  
Shan Lin ◽  
Jinhua Wang ◽  
Joseph P. Milazzo ◽  
Yali Xu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Acute Myeloid Leukemia ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Small Molecule ◽  
Myeloid Leukemia ◽  
Kinase Inhibition ◽  
Acute Myeloid ◽  
In Cells

Transcription factors are important drivers in acute myeloid leukemia (AML), but they are notoriously difficult to target. The authors demonstrate that inhibition of salt-inducible kinase (SIK3) inhibits AML cell proliferation in cells dependent on the transcription factor MEF2C, identifying a small molecule that can disrupt a leukemogenic transcription factor pathway.

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