The role of CDK1 siRNA interference in cell cycle and cell apoptosis

2009 ◽  
Vol 3 (4) ◽  
pp. 384-389 ◽  
Author(s):  
Hui Xiao ◽  
Ming Tian ◽  
Junna Ge ◽  
Xin Wei ◽  
Zhaoming Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Apoptosis ◽  
Sirna Interference

scholarly journals Deficiency of VCP-Interacting Membrane Selenoprotein (VIMP) Leads to G1 Cell Cycle Arrest and Cell Death in MIN6 Insulinoma Cells

2018 ◽  
Vol 51 (5) ◽  
pp. 2185-2197 ◽  
Author(s):  
Lili Men ◽  
Juan Sun ◽  
Decheng Ren
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Insulin Secretion ◽  
Cell Apoptosis ◽  
Β Cells ◽  
Β Cell ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest ◽  
Insulinoma Cells

Background/Aims: VCP-interacting membrane selenoprotein (VIMP), an ER resident selenoprotein, is highly expressed in β-cells, however, the role of VIMP in β-cells has not been characterized. In this study, we studied the relationship between VIMP deficiency and β-cell survival in MIN6 insulinoma cells. Methods: To determine the role of VIMP in β-cells, lentiviral VIMP shRNAs were used to knock down (KD) expression of VIMP in MIN6 cells. Cell death was quantified by propidium iodide (PI) staining followed by flow cytometric analyses using a FACS Caliber and FlowJo software. Cell apoptosis and proliferation were determined by TUNEL assay and Ki67 staining, respectively. Cell cycle was analyzed after PI staining. Results: The results show that 1) VIMP suppression induces β-cell apoptosis, which is associated with a decrease in Bcl-xL, and the β-cell apoptosis induced by VIMP suppression can be inhibited by overexpression of Bcl-xL; 2) VIMP knockdown (KD) decreases cell proliferation and G1 cell cycle arrest by accumulating p27 and decreasing E2F1; 3) VIMP KD suppresses unfolded protein response (UPR) activation by regulating the IRE1α and PERK pathways; 4) VIMP KD increases insulin secretion. Conclusion: These results suggest that VIMP may function as a novel regulator to modulate β-cell survival, proliferation, cell cycle, UPR and insulin secretion in MIN6 cells.

Costimulation with interleukin-4 and interleukin-10 induces mast cell apoptosis and cell-cycle arrest: the role of p53 and the mitochondrion

2004 ◽  
Vol 32 (12) ◽  
pp. 1137-1145 ◽  
Author(s):  
L. Andrew Bouton ◽  
Carlos D. Ramirez ◽  
Daniel P. Bailey ◽  
C. Fitzhugh Yeatman ◽  
Joyce Yue ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Mast Cell ◽  
Cell Cycle Arrest ◽  
Cell Apoptosis ◽  
Interleukin 10 ◽  
Interleukin 4 ◽  
Cycle Arrest

Influence of CDK1 and CDK2 siRNA interference on tumor cell cycle and cell apoptosis

2009 ◽  
Vol 8 (7) ◽  
pp. 371-374 ◽  
Author(s):  
Hui Xiao ◽  
Wanjun Gong ◽  
Jingpeng Cao ◽  
Xiaolan Li ◽  
Deding Tao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tumor Cell ◽  
Cell Apoptosis ◽  
Sirna Interference

scholarly journals circAPLP2 promotes colorectal cancer progression by upregulating HELLS by targeting miR-335-5p

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 338-350
Author(s):  
Rui Xiang ◽  
Min Feng ◽  
Xin Zhou ◽  
Lihong Ma ◽  
Ningfei Dong
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Tumor Growth ◽  
Nude Mice ◽  
Solid Tumor ◽  
Cell Apoptosis ◽  
Colony Formation ◽  
Cell Cycle Progression ◽  
Cycle Progression

Abstract Background Colorectal cancer (CRC) is one of the deadliest cancers in the world. Increasing evidence suggests that circular RNAs (circRNAs) are implicated in CRC pathogenesis. This study aimed to determine the role of circAPLP2 and explore a potential mechanism of circAPLP2 action in CRC. Methods The expression of circAPLP2, miR-335-5p and helicase lymphoid-specific (HELLS) mRNA in CRC tissues and cells was measured by quantitative real-time polymerase chain reaction (qPCR). The functional effects of circAPLP2 on cell cycle progression/cell apoptosis, colony formation, cell migration, invasion and glycolysis metabolism were investigated by flow cytometry assay, colony formation assay, wound healing assay, transwell assay and glycolysis stress test. Glycolysis metabolism was also assessed by the levels of glucose uptake and lactate production. The protein levels of HELLS and HK2 were detected by western blot. The interaction between circAPLP2 and miR-335-5p, or miR-335-5p and HELLS was verified by dual-luciferase reporter assay. The role of circAPLP2 on solid tumor growth in nude mice was investigated. Results circAPLP2 and HELLS were overexpressed, but miR-335-5p was downregulated in CRC tissues and cells. Functional analyses showed that circAPLP2 knockdown suppressed CRC cell cycle progression, colony formation, migration, invasion and glycolysis metabolism, induced cell apoptosis and blocked solid tumor growth in nude mice. Moreover, miR-335-5p was a target of circAPLP2, and miR-335-5p could also bind to HELLS. Rescue experiments presented that miR-335-5p inhibition reversed the effects of circAPLP2 knockdown, and HELLS overexpression abolished the role of miR-335-5p restoration. Importantly, circAPLP2 could positively regulate HELLS expression by mediating miR-335-5p. Conclusion circAPLP2 triggered CRC malignant development by increasing HELLS expression via targeting miR-335-5p, which might be a novel strategy to understand and treat CRC.

microRNA-133b Regulates Cell Proliferation and Cell Cycle Progression via Targeting HuR in Colorectal Cancer

2022 ◽  
Vol 12 (2) ◽  
pp. 335-345
Author(s):  
Xiaoyan Zhang ◽  
Wei Zhu ◽  
Junjie Lu
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cell Viability ◽  
Cell Lines ◽  
Cell Apoptosis ◽  
Quantitative Polymerase Chain Reaction ◽  
Luciferase Reporter ◽  
Protein Levels ◽  
Ht 29

MicroRNAs (miRNAs/miRs) have been identified to serve a key role in the development of tumors. However, the role of miR-133b in colorectal cancer (CRC) remains largely unclear. This study will investigate the role and mechanism of miR-133b in CRC. Reverse transcription-quantitative polymerase chain reaction analysis was performed to detect the level of miR-133b in CRC cell lines. Bioinformatics software TargetScan predicted the potential target genes of miR-133b, and a dual luciferase reporter assay was used to confirm this. To investigate the role of miR-133b in CRC cells, miR-133b was upregulated or downregulated in CRC cell lines (SW620 and HT-29) by transfecting with a miR-133b mimic or inhibitor, respectively. Subsequently, cell viability was analyzed using MTT assay, whereas cell apoptosis and the cell cycle distribution were analyzed by flow cytometry. In addition, the associated protein levels were detected using western blot analysis. The results demonstrated that miR-133b was significantly downregulated in CRC cell lines when compared with the normal colonic epithelial NCM-460 cell line. Human antigen R (HuR; also termed ELAVL1) was demonstrated to be a direct target of miR-133b and was negatively regulated by miR-133b. HuR was also notably upregulated in the CRC cell lines when compared with the normal control. Transfection of SW620 and HT-29 cells with the miR-133b mimic significantly inhibited cell viability, and induced cell apoptosis and G1 phase arrest, while upregulation of HuR demonstrated the opposite effects. Furthermore, the present data demonstrated that the miR-133b mimic significantly enhanced the protein levels of p21 and p27, and downregulated cyclin D1 and cyclin A levels in SW620 and HT-29 cells; the opposite effects were observed following treatment with the miR-133b inhibitor. In conclusion, the data indicate that miR-133b suppressed CRC cell growth by targeting HuR.

scholarly journals RNAi-mediated knockdown of MTNR1B without disrupting the effects of melatonin on apoptosis and cell cycle in bovine granulose cells

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e4463 ◽  
Author(s):  
Wenju Liu ◽  
Shujuan Wang ◽  
Jinxing Zhou ◽  
Xunsheng Pang ◽  
Like Wang
Keyword(s):  
Cell Cycle ◽  
Free Radical ◽  
Granulosa Cells ◽  
Cell Apoptosis ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Anti Oxidant ◽  
Granulose Cells ◽  
Apoptotic Pathways

Melatonin is well known as a powerful free radical scavenger and exhibits the ability to prevent cell apoptosis. In the present study, we investigated the role of melatonin and its receptor MTNR1B in regulating the function of bovine granulosa cells (GCs) and hypothesized the involvement of MTNR1B in mediating the effect of melatonin on GCs. Our results showed that MTNR1B knockdown significantly promoted GCs apoptosis but did not affect the cell cycle. These results were further verified by increasing the expression of pro-apoptosis genes (BAX and CASP3), decreasing expression of the anti-apoptosis genes (BCL2 and BCL-XL) and anti-oxidant genes (SOD1 and GPX4) without affecting cell cycle factors (CCND1, CCNE1 and CDKN1A) and TP53. In addition, MTNR1B knockdown did not disrupt the effects of melatonin in suppressing the GCs apoptosis or blocking the cell cycle. Moreover, MTNR1B knockdown did not affect the role of melatonin in increasing BCL2, BCL-XL, and CDKN1A expression, or decreasing BAX, CASP3, TP53, CCND1 and CCNE1 expression. The expression of MTNR1A was upregulated after MTNR1B knockdown, and melatonin promoted MTNR1A expression with or without MTNR1B knockdown. However, despite melatonin supplementation, the expression of SOD1 and GPX4 was still suppressed after MTNR1B knockdown. In conclusion, these findings indicate that melatonin and MTNR1B are involved in BCL2 family and CASP3-dependent apoptotic pathways in bovine GCs. MTNR1A and MTNR1B may coordinate the work of medicating the appropriate melatonin responses to GCs.

Fbxw11 Variants Promotes Proliferation of Leukemia Cells By Activating the NF-κB Signaling Pathway

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 894-894
Author(s):  
Lina Wang ◽  
Jinfeng Liao ◽  
Wenli Feng ◽  
Xiao Yang ◽  
Shayan Chen ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Leukemia Cells ◽  
Control Group ◽  
Over Expression

Abstract Fbxw11, as a member of F-box proteins family, is a constituent of the SCF (Skp1-Cul1-F box) ubiquitin ligase complex. This ligase ubiquitinates specifically phosphorylated substrates and controls the degradation and half-life of key cellular regulators. So, Fbxw11 play a pivotal role in many aspects of hematopoiesis and tumorigenesis through regulating various signal transduction pathways. We found two transcript variants (Fbxw11c and Fbxw11d) in mouse bone marrow. However the role of Fbxw11 variants in the development of leukemia and the underlying mechanisms remain largely unknown. In this study, we cloned three transcript variants (Fbxw11a, Fbxw11c and Fbxw11d) to study the biological function of Fbxw11 in leukemia. In order to investigate the role of Fbxw11 variants in leukemia, we established L1210 cell lines with over-expression of Fbxw11a, Fbxw11c and Fbxw11d respectively using the lentivirus system. The effect of Fbxw11 variants on proliferation of leukemia cells in vitro was first detected. Growth curve of leukemia cells with Fbxw11a, Fbxw11c or Fbxw11d over-expression was established by cell counting. The results suggested that over-expression of Fbxw11 variants stimulated the growth of leukemia cells. Then MTT experiment was carried out to study the effect of Fbxw11 variants on leukemia cell proliferation and the results showed that Fbxw11 variants increased the proliferation of L1210 cells in vitro. To further confirm the effects of Fbxw11 variants on proliferation of leukemia cells in vivo, tumor xenografts model with over-expression of Fbxw11a, Fbxw11c and Fbxw11d in DBA/2 mice was established. Leukemia cells L1210 with over-expression of Fbxw11a, Fbxw11c and Fbxw11d respectively were transplanted into DBA/2 mice by hypodermic injection. The tumor growth curves showed that tumor growth was increased in Fbxw11 variants over-expression group compared to the control group. Mice were sacrificed on day 28 after transplantation, greater volume of the xenograft tumors were obtained from Fbxw11 variants over-expression group than control group. Therefore, Over-expression of Fbxw11 variants could increase growth of tumor in vivo. To further investigate the molecular mechanism under the effect of Fbxw11 variants on proliferation of leukemia cells, we tested the apoptosis and cell cycle of leukemia cells with Fbxw11 variants over-expression. Over-expression of Fbxw11 variants did not affect the cell apoptosis but accelerated the process of cell cycle. These results revealed that the increased cell proliferation was not due to decrease in cell apoptosis but due to increase in cell cycle. In addition, we tested the effect of Fbxw11 variants on the signal transduction by dual-luciferase reporter gene system. The results showed that over-expression of Fbxw11 variants caused the activation of NF-κB signaling pathway. In conclusion, our findings suggest that Fbxw11 variants have promoting effect on cell proliferation of leukemia cells. The effect of Fbxw11 variants on cell proliferation are due to accelerated the process of cell cycle but not decreasing in cell apoptosis. Further study demonstrated that Fbxw11 variants promote cell proliferation through activating the NF-κB signaling pathway. The important role of Fbxw11 in regulating the development of leukemia suggests that a potent rationale for developing Fbxw11 as a potential therapeutic target against leukemia. Disclosures No relevant conflicts of interest to declare.

LncRNA Fetal-Lethal Noncoding Developmental Regulatory RNA (FENDRR) Suppresses Cell Proliferation and Promotes Apoptosis in Platelet Derived Growth Factor BB/Tumor Necrosis Factor α Induced Vascular Smooth Muscle Cells

2021 ◽  
Vol 11 (5) ◽  
pp. 912-919
Author(s):  
Xiaofang Chen ◽  
Dongjin Wang ◽  
Lingmei Qian
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Cell Apoptosis ◽  
Tumor Necrosis ◽  
Platelet Derived Growth Factor ◽  
Regulatory Rna ◽  
Necrosis Factor

Atherosclerosis is one of the primary causes that lead to cardiovascular disease. LncRNAs have been regarded as key modulators in many pathological processes. The study aims to identify the regulatory role of LncRNA fetal-lethal noncoding developmental regulatory RNA (FENDRR) in atherosclerosis. Cell viability proliferation, cell cycle and cell apoptosis were evaluated by Cell Counting Kit-8 (CCK-8) assay flow cytometric analysis and western blot analysis. Quantitative real-time PCR (qRT-PCR) was carried out to determine FENDRR expression in PDGF-BB/TNF-α induced VSMCs. Levels of TNF-α, IL-1, IL-6, MCP-1 and ICAM-1 were investigated by enzyme-linked immunosorbent assay (ELISA). The results showed that cell viability was enhanced and FENDRR expression was downregulated after VSMCs were induced by platelet derived growth factor BB (PDGF-BB) or tumor necrosis factor a (TNF-α). Cell proliferation was inhibited by FENDRR overexpression in a time-dependent manner in PDGF-BB or TNF-α induced VSMCs. Moreover, FENDRR overexpression blocked cell cycle, suppressed the generations of TNF-α, IL-1, IL-6, MCP-1 and ICAM-1, and facilitated cell apoptosis in VSMCs induced by PDGF-BB or TNF-α. These findings indicate the functional role of LncRNA FENDRR in atherosclerosis that attenuates cell proliferation and accelerates cell apoptosis.

Biological Role of CDK 11 and 12 in Cell Cycle and its Function in Tumorigenesis

2020 ◽  
Author(s):  
Shamim Mushtaq
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Web Of Science ◽  
The Body ◽  
Main Role ◽  
Hallmarks Of Cancer ◽  
Cyclin Dependent Kinases ◽  
Tumor Studies ◽  
Cycle Regulation

Uninhibited proliferation and abnormal cell cycle regulation are the hallmarks of cancer. The main role of cyclin dependent kinases is to regulate the cell cycle and cell proliferation. These protein kinases are frequently down regulated or up regulated in various cancers. Two CDK family members, CDK 11 and 12, have contradicting views about their roles in different cancers. For example, one study suggests that the CDK 11 isoforms, p58, inhibits growth of breast cancer whereas, the CDK 11 isoform, p110, is highly expressed in breast tumor. Studies regarding CDK 12 show variation of opinion towards different parts of the body, however there is a consensus that upregulation of cdk12 increases the risk of breast cancer. Hence, CDK 11 and CDK 12 need to be analyzed to confirm their mechanism and their role regarding therapeutics, prognostic value, and ethnicity in cancer. This article gives an outline on both CDKs of information known up to date from Medline, PubMed, Google Scholar and Web of Science search engines, which were explored and thirty relevant researches were finalized.

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