scholarly journals Fennel affects ovarian cell proliferation, apoptosis, and response to ghrelin

2021 ◽  
pp. 237-243
Author(s):  
AV Sirotkin ◽  
R Alexa ◽  
S Alwasel ◽  
AH Harrath
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Proliferation Marker ◽  
Direct Effects ◽  
Ovarian Cell ◽  
Animal Reproduction ◽  
Ovarian Cells ◽  
Proliferation And Apoptosis ◽  
Series Of Experiments ◽  
Apoptosis Marker

The objective of this study was to examine the direct effects of the medicinal plant fennel (Foeniculum vulgare Mill.) on basic functions of ovarian cells, including proliferation, apoptosis, and response to the physiological hormonal stimulator, ghrelin. In the first series of experiments, porcine ovarian granulosa cells were cultured with (1, 10, 100 µg/ml) or without fennel extract. In the second series of experiments, cells were cultured with (1, 10, 100 ng/ml) or without ghrelin, alone or in combination with fennel extract (10 µg/ml). Expression of the proliferation marker, PCNA, and the apoptosis marker, bax, were analyzed via quantitative immunocytochemical methods. Fennel stimulated the accumulation of the proliferation marker, and suppressed the expression of the apoptosis marker. Ghrelin alone promoted proliferation and apoptosis of ovarian cells. The presence of fennel inhibited these ghrelin effects. These observations provide the first demonstration of (1) effects of fennel on farm animal reproduction, (2) direct effects of fennel on ovarian cells, (3) the ability of fennel to promote ovarian cell proliferation, to inhibit ovarian cell apoptosis, and to enhance the ovarian cell proliferation:apoptosis ratio. Furthermore, our results (4) confirm the involvement of ghrelin in the control of ovarian cell apoptosis and proliferation, and (5) demonstrate the ability of fennel to affect not only ovarian cell proliferation and apoptosis, but also to suppress the responses of ovarian cells to the upstream hormonal regulator ghrelin. Our results indicate the potential applicability of fennel as a bio-stimulator of farm animal reproduction.

cAMP response element-binding protein 1 controls porcine ovarian cell proliferation, apoptosis, and FSH and insulin-like growth factor 1 response

2018 ◽  
Vol 30 (8) ◽  
pp. 1145 ◽  
Author(s):  
A. V. Sirotkin ◽  
A. Benčo ◽  
A. Tandlmajerová ◽  
M. Lauková ◽  
D. Vašíček ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Camp Response Element Binding ◽  
Insulin Like Growth Factor ◽  
Camp Response Element ◽  
Response Element ◽  
Ovarian Cell ◽  
Proliferation And Apoptosis ◽  
Element Binding Protein ◽  
Series Of Experiments

The aim of the present study was to examine the role of cAMP response element-binding protein (CREB) and its phosphorylation in the regulation of ovarian cell proliferation and apoptosis, and of the response of proliferation and apoptosis to the upstream hormonal stimulators FSH and insulin-like growth factor (IGF) 1. In the first series of experiments, porcine ovarian granulosa cells, transfected or not with a gene construct encoding wild-type CREB1 (CREB1WT), were cultured with and without FSH (0, 1, 10 or 100 ng mL−1). In the second series of experiments, these cells were transfected or not with CREB1WT or non-phosphorylatable mutant CREB1 (CREB1M1) and cultured with and without FSH (0, 1, 10 or 100 ng mL−1) or IGF1 (0, 1, 10 and 100 ng mL−1). Levels of total and phosphorylated (p-) CREB1, proliferating cell nuclear antigen (PCNA), a marker of proliferation, and BAX, a marker of apoptosis, were evaluated by western immunoblotting and immunocytochemical analysis. Transfection of cells with CREB1WT promoted accumulation of total CREB1 within cells, but p-CREB1 was not detected in any cell group. Both CREB1WT and CREB1M1 reduced cell proliferation and apoptosis. Addition of 10 and 100 ng mL−1 FSH to non-transfected cells promoted CREB1 accumulation and apoptosis, whereas cell proliferation was promoted by all concentrations of FSH tested. FSH activity was not modified in cells transfected with either CREB1WT or CREB1M1. IGF1 at 100 ng mL−1 promoted cell proliferation, whereas all concentrations of IGF1 tested reduced apoptosis. Transfection with either CREB1WT or CREB1M1 did not modify the effects of either FSH or IGF1, although CREB1M1 reversed the effect of IGF1 on apoptosis from inhibitory to stimulatory. These observations suggest that CREB1 is involved in the downregulation of porcine ovarian cell proliferation and apoptosis. The absence of visible CREB1 phosphorylation and the similarity between the effects of CREB1WT and CREB1M1 transfection indicate that phosphorylation is not necessary for CREB1 action on these processes. Furthermore, the observations suggest that FSH promotes both ovarian cell proliferation and apoptosis, whereas IGF1 has proliferation-promoting and antiapoptotic properties. The effect of FSH on CREB1 accumulation and the ability of CREB1M1 to reverse the effects of IGF1 on apoptosis indicate that CREB1 is a mediator of hormonal activity, but the inability of either CREB1WT or CREBM1transfection to modify the primary effects of FSH and IGF1 suggest that CREB1 and its phosphorylation do not mediate the action of these hormones on ovarian cell proliferation and apoptosis.

scholarly journals Resistin is a survival factor for porcine ovarian follicular cells

Reproduction ◽  
2015 ◽  
Vol 150 (4) ◽  
pp. 343-355 ◽  
Author(s):  
Agnieszka Rak ◽  
Eliza Drwal ◽  
Anna Wróbel ◽  
Ewa Łucja Gregoraszczuk
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Western Blot ◽  
Dna Fragmentation ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Inhibitory Effect ◽  
Ovarian Cell ◽  
Proliferation And Apoptosis ◽  
Mrna And Protein Expression

Previously, we demonstrated the expression of resistin in the porcine ovary, the regulation of its expression and its direct effect on ovarian steroidogenesis. The objective of this study was to examine the effect of resistin on cell proliferation and apoptosis in a co-culture model of porcine granulosa and theca cells. First, we analysed the effect of resistin at 1 and 10 ng/ml alone or in combination with FSH- and IGF1 on ovarian cell proliferation with an alamarBlue assay and protein expression of cyclins A and B using western blot. Next, the mRNA and protein expression of selected pro-apoptotic and pro-survival regulators of cell apoptosis, caspase-9, -8 and -3 activity and DNA fragmentation using real time PCR, western blot, fluorescent assay and an ELISA kit, respectively, were analysed after resistin treatment. Furthermore, we determined the effect of resistin on the protein expression of ERK1/2, Stat and Akt kinase. Using specific inhibitors of these kinases, we also checked caspase-3 activity and protein expression. We found that resistin, at both doses, has no effect on cell proliferation. The results showed that resistin decreased pro-apoptotic genes, which was confirmed on protein expression of selected factors. We demonstrate an inhibitory effect of resistin on caspase activity and DNA fragmentation. Finally, resistin stimulated phosphorylation of the ERK1/2, Stat and Akt and kinases inhibitors reversed resistin action on caspase-3 activity and protein expression to control. All of these results showed that resistin has an inhibitory effect on porcine ovarian cell apoptosis by activation of the MAPK/ERK, JAK/Stat and Akt/PI3 kinase signalling pathways.

LncRNA LINC00858 enhances cervical cancer cell growth through miR-3064-5p/ VMA21 axis

2021 ◽  
pp. 1-11
Author(s):  
Min Wei ◽  
Youguo Chen ◽  
Wensheng Du
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Luciferase Reporter ◽  
Cancer Cell Growth ◽  
Protein Coding ◽  
Gynecological Malignancy ◽  
Promising Therapeutic Target ◽  
Proliferation And Apoptosis ◽  
Reporter Assays

BACKGROUND: Cervical cancer (CC) is the most common form of gynecological malignancy. Long intergenic non-protein coding RNA 858 (LINC00858) has been identified to participate in multiple cancers. However, the role and mechanism of LINC00858 in CC cells are still elusive. AIM: The aim of this study is to explore the biological functions and mechanisms of LINC00858 in CC cells. METHODS: RT-qPCR analysis was used to examine the expression of LINC00858 in CC cells. EdU and colony formation assay were utilized to assess cell proliferation. TUNEL assay and flow cytometry assay were conducted to assess cell apoptosis. The mechanism regarding LINC00858 was certified through RNA pull down, RIP and luciferase reporter assays. RESULTS: The up-regulated LINC00858 was detected in CC cells. Reduction of LINC00858 effectively subdued CC cells proliferation and stimulated cell apoptosis. LINC00858 was determined to bind with miR-3064-5p and up-regulate VMA21 in CC cells. In rescue assays, miR-3064-5p down-regulation and VMA21 up-regulation were able to counteract the effect caused by LINC00858 decrease on CC cell proliferation and apoptosis. CONCLUSION: LINC00858 enhances cell proliferation, while restraining cell apoptosis in CC through targeting miR-3064-5p/VMA21 axis, implying that LINC00858 may serve as a promising therapeutic target for CC.

Effects of Simvastatin on Breast Carcinoma Cell Proliferation and Apoptosis via Transforming Growth Factor-β1/Smad3 Pathway

2021 ◽  
Vol 11 (9) ◽  
pp. 1673-1682
Author(s):  
Feng Wang ◽  
Gengbao Qu ◽  
Baokai Wang
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Breast Carcinoma ◽  
Protein Expression ◽  
Breast Cancer Cell ◽  
Cell Apoptosis ◽  
Carcinoma Cell ◽  
Proliferation And Apoptosis ◽  
Smad3 Protein ◽  
Mcf 7

Objective: To investigate the function and causative role of simvastatin (Sim) in breast carcinoma cell apoptosis as well as proliferation. Methods: 20 breast carcinoma patients requiring surgery were treated with Sim (20 days, 30 mg), and samples of pre-treatment (pre) and post-treatment (post) were acquired. We detected tissue cell proliferation and apoptosis changes and used functional experiments to detect cell proliferation and apoptosis changes after treating not only estrogen receptor (ER)-positive (MCF-7) but also ER-negative cells (MDA-MB-231) with Sim or TGF-β1. Detection of p-Smad3 and total Smad3 protein expression changes was conducted, and we finally used in vivo experiments to assess the influence of Sim on breast tumor growth and drug safety. Results: Immunohistochemistry and TUNEL staining results showed that after treatment with Sim, breast carcinoma cell proliferation decreased and apoptosis increased. Functional experiments results showed that Sim notedly promoted the MDA-MB-231 and MCF-7 cell apoptosis, inhibiting migration, proliferation and epithelial mesenchymal transition. Moreover, TGF-β1 protein expression was strikingly lower in Sim group than that in DMSO group. When TGF-β1 and Sim were combined to use, the inhibitory ability of Sim on breast cancer cell proliferation markedly increased and the capability of TGF-β1 protein inducing p-Smad3 protein increased. In addition, after Sim treatment in mice, the tumor volume became smaller, the pathological changes weakened, and there was no significant effect on liver function and kidney function. Conclusion: Sim participates in breast cancer cell apoptosis and proliferation via regulating TGF-β1/Smad3 signal pathway.

Effects of miR-1305 on Proliferation and Apoptosis of Non-Small Cell Lung Cancer Cells via Regulating High Mobility Group Box-1 Level

2020 ◽  
Vol 10 (12) ◽  
pp. 1837-1842
Author(s):  
Wenpu Zhao ◽  
Xiaolian Yang ◽  
Yishan Dong ◽  
Jin Quan ◽  
Li Huang
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cell Apoptosis ◽  
Mrna Level ◽  
Small Cell ◽  
Small Cell Lung ◽  
Hmgb1 Level ◽  
Proliferation And Apoptosis

Abnormal expression of HMGB1 is closely related to non-small cell lung cancer (NSCLC). miR-1305 regulates HMGB1 level by MiRDB analysis. Therefore, we investigated whether miR-1305 affects NSCLC cell proliferation and apoptosis by regulating HMGB1. The control group (NC group), miR-1305 Mimics group and miR-1305 Mimics+pcDNA-HMGB1 group were set followed by analysis of miR-1305 and HMGB1 mRNA level real time-PCR, relationship between miR-1305 and HMGB1 by dual fluorescein reporter assay, HMGB1 and Tubulin level by Western blot, cell proliferation by clone formation assay, cell apoptosis by Annexin V-FITC/PI staining. Compared with normal tissues, miR-1305 was significantly downregulated in NSCLC tissues (P <0.01), while HMGB1 mRNA was upregulated (P <0.01). HMGB1 was the target gene of miR-1305. Compared to NC group, HMGB1 level in miR-1305 Mimics group was significantly reduced (P <0.01). Compared with miR-1305 Mimics group, HMGB1 level was significantly increased in miR-1305 Mimics+pcDNA-HMGB1group (P <0.05). HMGB1 mRNA level was not significantly changed. In addition, the number of cell clones and proliferation ability was decreased in miR-1305 Mimics group, which were reversed in miR-1305 Mimics+pcDNA-HMGB1 group. miR-1305 can bind HMGB1 3′-UTR, reduce its protein level, thereby inhibiting NSCLC cell proliferation and promoting cell apoptosis. HMGB1 overexpression can prevent the effect of miR-1305.

S100A4 promotes the progression of lipopolysaccharide-induced acute epididymitis in mice†

2020 ◽  
Vol 102 (6) ◽  
pp. 1213-1224 ◽  
Author(s):  
Yingjie Wu ◽  
Haoran Li ◽  
Yinghe Qin
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Mrna Levels ◽  
Ki 67 ◽  
Tnf Α ◽  
Proliferation And Apoptosis ◽  
Sperm Membrane ◽  
Marked Cell ◽  
Acute Epididymitis

Abstract S100A4 has been suggested to be a critical regulator of tumor metastasis and is implicated in the progression of inflammation. The aim of this study is to investigate the expression and possible role of S100A4 in epididymitis. Using a mouse model of epididymitis induced by the injection of lipopolysaccharide (LPS) in the deferent duct, we found that LPS administration induced an upregulation of S100a4 transcription (P &lt; 0.05) and a recruitment of S100A4 positive cells in the epididymal interstitium of wild type (WT) mice. Co-immunofluorescence showed that S100A4 was mainly expressed by granulocytes, CD4 lymphocytes, and macrophages. Deficiency of S100A4 reduced epididymal pathological reaction and the mRNA levels of the pro-inflammatory cytokines IL-1β and TNF-α (P &lt; 0.01), suggesting that S100A4 promotes the progression of epididymitis. Furthermore, S100A4 deficiency alleviated the decline of sperm motility and rectified the abnormal expression of sperm membrane protein AMAD3, which suggested that in the progression of epididymitis, S100A4 aggravates the damage to sperm vitality. In addition, both Ki-67 marked cell proliferation and transferase-mediated dUTP-biotin nick end labeling detected cell apoptosis were reduced in S100a4−/− mice compared with WT mice after LPS treatment, indicating that S100A4 promotes both cell proliferation and cell apoptosis in epididymitis. Overall, these results demonstrate that S100A4 promotes the progression of LPS-induced epididymitis and facilitates a decline in sperm vitality, and its function may be related to the process of cell proliferation and apoptosis during inflammation.

miR-124 Regulates Caveolin-1 Expression and Affects Proliferation and Apoptosis of Osteosarcoma Cells

2019 ◽  
Vol 9 (9) ◽  
pp. 1245-1249
Author(s):  
Huanzhi Ma ◽  
Jian Wang ◽  
Jun Shi ◽  
Wei Zhang ◽  
Dongsheng Zhou
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Luciferase Activity ◽  
Cell Number ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Specific Mechanism ◽  
Caveolin 1 ◽  
Proliferation And Apoptosis ◽  
Relative Luciferase Activity

Osteosarcoma (OS) seriously affects human health. miR-124 expression is closely related to osteosarcoma, but its specific mechanism remains unclear. Our study intends to evaluate miR-124’s effect on osteosarcoma. MG-63 cells were transfected with miR-124 mimics/NC followed by analysis of miR-124 expression by real-time PCR, cell proliferation by CCK8 assay, cell apoptosis by flow cytometry as well as the level of caveolin-1 (CAV1) by Western blot. miR-124 was significantly lower and CAV1 was increased in the four osteosarcoma cells than those in normal osteoblasts (P < 0.05). miR-124 mimics transfection significantly reduced CAV1 level and cell number (P < 0.05) and increased cell apoptosis rate (P < 0.05). Moreover, miR-124 inhibitor significantly promoted the relative luciferase activity in pmirGLO-CAV1-3′UTR-wt-transfected cells (P < 0.05). miR-124 affects osteosarcoma cell proliferation and apoptosis via targeting CAV1.

miR-203 Regulates Proliferation and Apoptosis of Colorectal Cancer Cells Through Targeting DJ-1

2020 ◽  
Vol 10 (3) ◽  
pp. 365-370
Author(s):  
Qiupeng Du ◽  
Na Du ◽  
Chenchen Zhu ◽  
Qingqing Shang ◽  
Haiyan Mao ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Akt Signaling ◽  
Pten Expression ◽  
Proliferation And Apoptosis ◽  
Colorectal Cancer Cells ◽  
Colorectal Cell ◽  
Sw480 Cells

Objective: To assess whether miR-203 regulates DJ-1 expression, affects colorectal cancer cells through PTEN-PI3K/AKT signaling. Methods: Colorectal cancer (CRC) tissues and adjacent tissues were collected followed by analysis of the level of miR-203, DJ-1 and PTEN. miR-203 and DJ-1 level was measured in HCT116, SW480 and normal colorectal cell NCM460. miR-203 mimic or miR-NC was transfected into HCT116 or SW480 cells followed by measuring the level of miR-203, DJ-1, PTEN, p-AKT as well as cell apoptosis and proliferation. Results: Compared with tumor adjacent tissues, tumor tissues showed significantly lower level of miR-203 and PTEN, and higher level of DJ-1. There is a targeted relationship between miR-203 and DJ-1. Compared with NCM460 cell, HCT116 and SW480 cells displayed significantly lower miR-203 level and higher DJ-1 expression. miR-203 mimic significantly reduced DJ-1 and p-AKT level, increased PTEN expression, cell apoptosis and inhibited cell proliferation. Conclusion: Lower miR-203 and higher DJ-1 level is found in CRC patients. Upregulation of miR-203 inhibits DJ-1 expression, increases PTEN expression, impairs PI3K/AKT signaling, inhibits CRC cell proliferation and promotes apoptosis.

scholarly journals The Long Non-Coding RNA SNHG16 Promotes NPC Cell Progression by Competitively Binding miR-23b-3p

2020 ◽  
Author(s):  
Hou Wei ◽  
Lu Xu ◽  
Tao Su ◽  
Yunxiao Wu ◽  
Yujuan Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Luciferase Reporter ◽  
Reporter System ◽  
Qrt Pcr ◽  
Non Coding Rna ◽  
Proliferation And Apoptosis ◽  
Two Factors ◽  
Cell Progression ◽  
Long Non Coding Rna

Abstract Background: This study aims at verifying the effect of non-coding RNA SNHG16 on promotes NPC cell progression via binding miR-23b-3p.Methods: The expression of non-coding RNA SNHG16 was detected by qRT-PCR in cell lines including c666-1 and HONE-1. Si-MCM6 and si-SNHG16 are transfected to cells to verify their effects on cell proliferation and apoptosis. MTT is used to measure cell viability while flow cytometry assay and transwell assay were used for cell apoptosis, cell cycle and invasion respectively. The expression level of MCM6 was determined by western blot. Relationships between mRNA MCM6 and lncRNA SNHG16 were explored by qRT-PCR and nude mouse tumorigenicity assay.Results: The MCM6 was overexpressed in NPC tissues and lncRNA SNHG16 showed the same trend. Those two factors were correlated with high cancer stage. The expression of MCM6 was decreased after si-SNHG16 and dual luciferase reporter system demonstrated their combine with miR-23b-3p. Further we explored the down-regulation of lncRNA SNHG16 could inhibit NPC cell proliferation, colony formation and also accelerate cell apoptosis rate. And this result could be altered by adding miR-23b-3p inhibitor.Conclusion: The lncRNA SNHG16 is able to promote the NPC proliferation via binding miR-23b-3p, which has potential for future treatment.

scholarly journals PSAT1 prompted cell proliferation and inhibited cell apoptosis in multiple myeloma through regulating PI3K/AKT pathway

2020 ◽  
Vol 19 (4) ◽  
pp. 745-749
Author(s):  
Hongqing Zhu ◽  
Yejun Si ◽  
Yun Zhuang ◽  
Meng Li ◽  
Jianmin Ji ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Underlying Mechanism ◽  
Akt Pathway ◽  
Protein Levels ◽  
Phosphoserine Aminotransferase ◽  
Proliferation And Apoptosis ◽  
Mrna And Protein Expression ◽  
Polymerase Chain

Purpose: To identify the biological function of phosphoserine aminotransferase 1 (PSAT1) in regulating cell proliferation and apoptosis in multiple myeloma (MM).Methods: The mRNA and protein levels of PSAT1 were determined using quantitative real-time polymerase chain reaction (PCR) and western blotting, respectively. Cell proliferation was measured using CCK-8 assay.Results: PSAT1 mRNA and protein expression levels were significantly increased in MM cell lines when compared to control cells. Moreover,  downregulation of PSAT1 inhibited MM cell proliferation and induced cell apoptosis, whereas overexpression of PSAT1 promoted MM cell  proliferation and suppressed cell apoptosis. Further analysis demonstrated that the underlying mechanism was via regulation of PI3K/AKT pathway.Conclusion: The results identified a novel role for PSAT1 in the progression of MM, which may provide a therapeutic and a new anticancer target for the therapy of MM. Keywords: Multiple myeloma, PSAT1, Cell proliferation, PI3K/AKT pathway

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