scholarly journals Promotion of BZW2 by LINC00174 through miR-4500 inhibition enhances proliferation and apoptosis evasion in laryngeal papilloma

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Jiajia Liu ◽  
Tao Yang ◽  
Ying Zhang ◽  
Shuhui Wang
Keyword(s):  
Cell Proliferation ◽  
Human Papillomavirus ◽  
Cell Apoptosis ◽  
Leucine Zipper ◽  
Target Genes ◽  
Laryngeal Papillomatosis ◽  
Basic Leucine Zipper ◽  
Laryngeal Papilloma ◽  
Protein Levels ◽  
Proliferation And Apoptosis

Abstract Background We aimed to explore the roles of basic leucine zipper and W2 domains (BZW) 2 in the human papillomavirus-infected laryngeal papillomatosis. Methods In the present study, BZW 2 knockdown and overexpressed cell lines were constructed. CCK-8 and colony formation assays were used to determine cell proliferation. Caspase-3 activity and nucleosomes fragmentation assays were used to determine cell apoptosis. qRT-PCR and Western blot were employed to evaluate the mRNA and protein levels of target genes, respectively. Luciferase and biotin-coupled miRNA pulldown assays were used to examine the interactions between mRNA and mRNA. Results We observed the levels of BZW2 were up-regulated in the laryngeal papilloma (LP) tissues as compared with adjacent tissues. The knockdown of BZW2 significantly inhibited cell proliferation and promoted cell apoptosis in the LP cells. Additionally, we identified the expressions of BZW2 negatively regulated by miR-4500. Luciferase and biotin-coupled miRNA pulldown assays demonstrated that LINC00174 competed with the BZW2 for binding with miR-4500. Moreover, the results showed that LINC00174/miR-4500/BZW2 axis regulated cell proliferation and apoptosis. Conclusion Our results demonstrated that the regulation of LINC00174/miR-4500/BZW2 axis might be used as an effective strategy for treatment of human papillomavirus-infected laryngeal papillomatosis.

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

scholarly journals Effects of ODC on Polyamine Metabolism, Hormone Levels, Cell proliferation and Apoptosis in Goose Ovarian Granulosa Cells

2020 ◽  
Author(s):  
Chunyang Niu ◽  
Sujuan Zhang ◽  
Guilin Mo ◽  
Yilong Jiang ◽  
Liang Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Granulosa Cell ◽  
Granulosa Cells ◽  
Cell Apoptosis ◽  
Culture Medium ◽  
Polyamine Metabolism ◽  
Hormone Levels ◽  
Apoptosis Rate ◽  
Protein Levels ◽  
Proliferation And Apoptosis

Abstract Background: Ornithine decarboxylase (ODC) plays an indispensable role in the process of polyamine biosynthesis. Polyamines are a pivotal part of living cells and have diverse roles in the regulation of cell proliferation and apoptosis, aging and reproduction. However, to date, there have been no reports about ODC regulating follicular development in goose ovaries. Here, we constructed ODC siRNA and overexpression plasmids and transfected them into goose primary granulosa cells (GCs) to elucidate the effects of ODC interference and overexpression on the polyamine metabolism, hormone levels, cell apoptosis and proliferation of granulosa cells.Results: After interfering with ODC in GCs, the mRNA and protein levels of ODC and the content of putrescine were greatly decreased (P < 0.05). When ODC was overexpressed, ODC mRNA and protein levels and putrescine content were greatly increased (P < 0.05). The polyamine-metabolizing enzyme genes OAZ1 and SSAT were significantly increased, and SPDS was significantly decreased when ODC was downregulated (P < 0.05). OAZ1, SPDS and SSAT were significantly increased when ODC was upregulated (P < 0.05). In addition, after interference with ODC, P4 (progesterone) levels in the culture medium of GCs increased greatly (P < 0.05), while the overexpression of ODC caused the P4 level to decrease significantly (P < 0.05). After ODC downregulation, granulosa cell activity was significantly reduced, the apoptosis rate was significantly increased, and the BCL-2/BAX ratio was downregulated (P < 0.05). Under ODC overexpression, the activity of GCs was notably increased, the apoptosis rate was significantly reduced, and the BCL-2/BAX protein ratio was upregulated (P < 0.05).Conclusions: Our study successfully induced ODC interference and overexpression in goose ovarian GCs, and ODC regulated mainly putrescine content in GCs with a slight influence on spermidine and spermine. Moreover, ODC participated in the adjustment of P4 levels in the culture medium of GCs, promoted granulosa cell proliferation and inhibited granulosa cell apoptosis.

scholarly journals MPP8 Promotes Proliferation and Restrains Apoptosis in Osteosarcoma by Regulating p38αMAPK Pathway

2021 ◽  
Vol 20 ◽  
pp. 153303382199527
Author(s):  
Tao Li ◽  
Na Li ◽  
Lei Wang ◽  
Jia Li ◽  
Xin Zhang
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
In Vitro Study ◽  
Underlying Mechanism ◽  
Osteosarcoma Cell ◽  
Protein Levels ◽  
Proliferation And Apoptosis ◽  
M Phase ◽  
Primary Bone

Osteosarcoma is the most common primary bone malignancy. We aim to investigate that role of M-phase phosphoprotein 8 (MPP8) on proliferation and apoptosis in osteosarcoma. Briefly, the current research reported an in vitro study investigating the role MPP8 in OS tumorigenesis. Consequently, we found that the MPP8 expression was upregulated in osteosarcoma tissues and in osteosarcoma cell lines. Interestingly, MPP8 knockdown via shRNA restrained the cell viability and proliferation of U2OS and Saos-2 cells. In addition, MPP8 knockdown promoted the apoptosis of U2OS and Saos-2 cells, while MPP8 overexpression promotes proliferation and inhibited the cell apoptosis of osteosarcoma cells. These results suggested that MPP8 may serve as a contributor for osteosarcoma growth and inhibition of MPP8 may help restrain the development of osteosarcoma. Importantly, we found that MPP8 overexpression suppressed the protein levels of HOXA5, p38αMAPK, increased cell proliferation and inhibited cell apoptosis, while co-transfection with HOXA5 overexpression suppressed the cell proliferation and increased cell apoptosis. These results indicated that MPP8 contributed to cell proliferation and the underlying mechanism might be involved with HOXA5/ p38αMAPK pathway.

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.

FOXD3 inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinoma through regulation of the PI3K–Akt pathway

2020 ◽  
Vol 98 (6) ◽  
pp. 653-660 ◽  
Author(s):  
Xiaoxing Xie ◽  
Gaoyun Xiong ◽  
Wenjun Chen ◽  
Hongdan Fu ◽  
Mingqian Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Nasopharyngeal Carcinoma ◽  
Cell Apoptosis ◽  
Inhibitory Effect ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Inhibitory Effects ◽  
Protein Levels ◽  
Flow Cytometric ◽  
Phosphoinositide 3 Kinase

FOXD3 has been found previously to positively regulate miR-26b, a tumor inhibitor of nasopharyngeal carcinoma (NPC). However, FOXD3’s precise function and associated mechanism of action in NPC have not yet been investigated. In this study, the expression of FOXD3 mRNA and protein was evaluated using RT-qPCR, western blotting, and immunohistochemistry. Protein levels involved in the phosphoinositide 3-kinase – protein kinase B (PI3K–Akt) pathway were assessed by western blot, and cell proliferation was determined by MTT and colony forming assays. Additionally, cell apoptosis was assessed by flow cytometric assay. Finally, the migration and invasion capabilities of the NPC cells were determined using wound healing and Transwell assays. We found that FOXD3 levels were relatively low in NPC tissue and cells, while an increase caused the inhibition of the PI3K–Akt pathway. Functional experiments found that overexpression of FOXD3 suppressed cell proliferation, migration, and invasion and enhanced cell apoptosis in NPC C6661 cells. IGF-1, an activator of the PI3K–Akt pathway, reversed the inhibitory effect of FOXD3. Furthermore, we found upregulation of the PI3K–Akt pathway and upregulation of the inhibitory effects of FOXD3 on C6661 cellular activities. In conclusion, FOXD3 negatively affected the PI3K–Akt pathway to restrain the processes involved in C6661 cell pathology. These findings further exposed the function and downstream axis of FOXD3 in NPC and displayed a promising new target for NPC therapy.

scholarly journals Rsf-1 Influences the Sensitivity of Non-Small Cell Lung Cancer to Paclitaxel by Regulating NF-κB Pathway and Its Downstream Proteins

2017 ◽  
Vol 44 (6) ◽  
pp. 2322-2336 ◽  
Author(s):  
Xitao Chen ◽  
Xiaodi Sun ◽  
Jingqian Guan ◽  
Junda Gai ◽  
Jilin Xing ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Flow Cytometry ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Apoptosis ◽  
Small Cell ◽  
Small Cell Lung ◽  
Protein Levels ◽  
H460 Cell ◽  
Xenograft Mice

Background/Aims: The therapeutic efficacy of paclitaxel is hampered by chemotherapeutic resistance in non-small cell lung cancer (NSCLC). Rsf-1 enhanced paclitaxel resistance via nuclear factor-κB (NF-κB) in ovarian cancer cells and nasopharyngeal carcinoma. This study assessed the function of Rsf-1 in the modulation of the sensitivity of NSCLC to paclitaxel via the NF-κB pathway. Methods: The mRNA and protein levels of the related genes were quantified by RT-PCR and Western blotting. Rsf-1 silencing was achieved with CRISPR/Cas9 gene editing. Cell cycle, migration and proliferation were tested with flow cytometry, transwell test and CCK8 test. Cell apoptosis was analyzed with flow cytometry and quantification of C-capase3. The parameters of the tumors were measured in H460 cell xenograft mice. Results: Rsf-1 was highly expressed in H460 and H1299 cells. Rsf-1 knockout caused cell arrest at the G1 phase, increased cell apoptosis, and decreased migration and cell proliferation. Rsf-1 knockout increased the inhibition of cell proliferation, the reduction in cell migration and the augment in cell apoptosis in paclitaxel treated H460 and H1299 cells. Rsf-1 knockout further enhanced the paclitaxel-mediated decrease in the volume and weight of the tumors in H460 cell xenograft mice. Helenalin and Rsf-1 knockout decreased the protein levels of p-P65, BcL2, CFLAR, and XIAP; hSNF2H knockout decreased the protein level of NF-κB p-P65 without altering Rsf-1 and p65 protein levels, while Rsf-1 and hSNF2H double knockout decreased the level of NF-κB p-P65, in H1299 and H460 cells. Conclusion: These results demonstrate that Rsf-1 influences the sensitivity of NSCLC to paclitaxel via regulation of the NF-κB pathway and its downstream genes.

scholarly journals Identification of New miRNA-mRNA Networks in the Development of Non-syndromic Cleft Lip With or Without Cleft Palate

2021 ◽  
Vol 9 ◽  
Author(s):  
Chengyi Fu ◽  
Shu Lou ◽  
Guirong Zhu ◽  
Liwen Fan ◽  
Xin Yu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cleft Palate ◽  
Negative Correlation ◽  
Cell Apoptosis ◽  
Cleft Lip ◽  
Target Genes ◽  
Craniofacial Development ◽  
Differentially Expressed ◽  
Differentially Expressed Mirnas

Objective: To identify new microRNA (miRNA)-mRNA networks in non-syndromic cleft lip with or without cleft palate (NSCL/P).Materials and Methods: Overlapping differentially expressed miRNAs (DEMs) were selected from cleft palate patients (GSE47939) and murine embryonic orofacial tissues (GSE20880). Next, the target genes of DEMs were predicted by Targetscan, miRDB, and FUNRICH, and further filtered through differentially expressed genes (DEGs) from NSCL/P patients and controls (GSE42589), MGI, MalaCards, and DECIPHER databases. The results were then confirmed by in vitro experiments. NSCL/P lip tissues were obtained to explore the expression of miRNAs and their target genes.Results: Let-7c-5p and miR-193a-3p were identified as DEMs, and their overexpression inhibited cell proliferation and promoted cell apoptosis. PIGA and TGFB2 were confirmed as targets of let-7c-5p and miR-193a-3p, respectively, and were involved in craniofacial development in mice. Negative correlation between miRNA and mRNA expression was detected in the NSCL/P lip tissues. They were also associated with the occurrence of NSCL/P based on the MGI, MalaCards, and DECIPHER databases.Conclusions: Let-7c-5p-PIGA and miR-193a-3p-TGFB2 networks may be involved in the development of NSCL/P.

scholarly journals Regulation of Nitrate (NO3) Transporters and Glutamate Synthase-Encoding Genes under Drought Stress in Arabidopsis: The Regulatory Role of AtbZIP62 Transcription Factor

Plants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2149
Author(s):  
Nkulu Kabange Rolly ◽  
Byung-Wook Yun
Keyword(s):  
Transcription Factor ◽  
Drought Stress ◽  
Leucine Zipper ◽  
Target Genes ◽  
De Novo ◽  
In Silico Analysis ◽  
Glutamate Synthase ◽  
Regulatory Elements ◽  
Transcript Accumulation ◽  
Basic Leucine Zipper

Nitrogen (N) is an essential macronutrient, which contributes substantially to the growth and development of plants. In the soil, nitrate (NO3) is the predominant form of N available to the plant and its acquisition by the plant involves several NO3 transporters; however, the mechanism underlying their involvement in the adaptive response under abiotic stress is poorly understood. Initially, we performed an in silico analysis to identify potential binding sites for the basic leucine zipper 62 transcription factor (AtbZIP62 TF) in the promoter of the target genes, and constructed their protein–protein interaction networks. Rather than AtbZIP62, results revealed the presence of cis-regulatory elements specific to two other bZIP TFs, AtbZIP18 and 69. A recent report showed that AtbZIP62 TF negatively regulated AtbZIP18 and AtbZIP69. Therefore, we investigated the transcriptional regulation of AtNPF6.2/NRT1.4 (low-affinity NO3 transporter), AtNPF6.3/NRT1.1 (dual-affinity NO3 transporter), AtNRT2.1 and AtNRT2.2 (high-affinity NO3 transporters), and AtGLU1 and AtGLU2 (both encoding glutamate synthase) in response to drought stress in Col-0. From the perspective of exploring the transcriptional interplay of the target genes with AtbZIP62 TF, we measured their expression by qPCR in the atbzip62 (lacking the AtbZIP62 gene) under the same conditions. Our recent study revealed that AtbZIP62 TF positively regulates the expression of AtPYD1 (Pyrimidine 1, a key gene of the de novo pyrimidine biosynthesis pathway know to share a common substrate with the N metabolic pathway). For this reason, we included the atpyd1-2 mutant in the study. Our findings revealed that the expression of AtNPF6.2/NRT1.4, AtNPF6.3/NRT1.1 and AtNRT2.2 was similarly regulated in atzbip62 and atpyd1-2 but differentially regulated between the mutant lines and Col-0. Meanwhile, the expression pattern of AtNRT2.1 in atbzip62 was similar to that observed in Col-0 but was suppressed in atpyd1-2. The breakthrough is that AtNRT2.2 had the highest expression level in Col-0, while being suppressed in atbzip62 and atpyd1-2. Furthermore, the transcript accumulation of AtGLU1 and AtGLU2 showed differential regulation patterns between Col-0 and atbzip62, and atpyd1-2. Therefore, results suggest that of all tested NO3 transporters, AtNRT2.2 is thought to play a preponderant role in contributing to NO3 transport events under the regulatory influence of AtbZIP62 TF in response to drought stress.

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.

Sign in / Sign up

Export Citation Format

Share Document