scholarly journals Effect of Daidzein on the Proliferation of Lung Cancer Cells Involved in the Apoptotic Signaling Pathway

2020 ◽  
Author(s):  
Hui Liu ◽  
Xiaobo Wang ◽  
Ouyang Jin ◽  
Denggang Fu ◽  
You Peng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Signaling Pathway ◽  
Tp53 Gene ◽  
Cell Counting ◽  
Pcr Analysis ◽  
Human Embryonic Lung ◽  
Bioactive Substances ◽  
Apoptosis Pathway ◽  
Wide Range ◽  
Proliferation And Apoptosis

Abstract Background: Daidzein is one of the key bioactive substances of soybean isoflavones that has a wide range of health benefits includes antineoplastic. Epidemiological evidence suggests that soy glycogen is associated with the incidence and prognosis of lung cancer. we purposed to assess the effect and molecular mechanism of daidzein on lung cancer, and to maximize therapy outcome for individualized treatment. Methods: In this report, H1299 were cultured in a medium with 10 μM daidzein for 6 hours , we detected the expression level of apoptosis-related genes in H1299 by cDNA microarray analysis. The selected genes were further validated by using RT-PCR analysis and Western blot. Finally, We usedflow cytometry to detect cell cycle alterations, and apoptosis the proliferation and apoptosis in HELF and H1299 cells were detected by Cell counting kit-8 assays. Results: These results indicate that low concentrations of isoflavone crude extract and daidzein could significantly affect the proliferation of H1299 (Human lung adenocarcinoma) and HELF (Human embryonic lung fibroblast) cells. The results of microarray in our study suggest that apoptosis-related genes are up-regulated induced by daidzein in H1299 cells and verified by RT-qPCR, particularly TP53 and caspase9. Western blotting shows the effect of daidzein on P53 and caspase9 in HELF cells be more obvious than it in H1299 cells. While the expression of TP53 was suppressed by pifithrin-α (PFTα) in HELF and H1299 cells, the mRNA and protein expression of TP53 still increase induced by daidzein, also, the effect of apoptosis induced by daidzein is involved in the P53 apoptosis pathway through inhibition of TP53 gene expression by PFTα. Conclusions: In conclusion, daidzein affected proliferation and apoptosis in HELF and H1299 cells, and the mechanism of apoptosis involved in the P53 signaling pathway.

scholarly journals COPB2 gene silencing inhibits colorectal cancer cell proliferation and induces apoptosis via the JNK/c-Jun signaling pathway

PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0240106
Author(s):  
Yan Wang ◽  
Guangmei Xie ◽  
Min Li ◽  
Juan Du ◽  
Min Wang
Keyword(s):  
Colorectal Cancer ◽  
Gene Silencing ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Cell Counting ◽  
Apoptosis Pathway ◽  
Proliferation And Apoptosis ◽  
Related Proteins ◽  
Hct116 Cells

Objectives Colorectal cancer (CRC) is one of the most common malignant human tumors. It is associated with high morbidity and mortality rates. In recent years, tumor gene therapy has emerged as a promising new approach for colorectal cancer therapy. Herein, we identify and analyze the role of COPB2 (coatomer protein complex, subunit beta 2) in proliferation and apoptosis of CRC cells. Methods To investigate the role of COPB2 in the proliferation and apoptosis of CRC cells, a shCOPB2 vector and a shCtrl vector were constructed for transfection into RKO and HCT116 cells. Cells proliferation was subsequently measured via cell counting kit-8 (CCK8) assay and Celigo cell counting assay. Apoptosis was measured via flow cytometry. The activity level of Caspase 3/7 was measured. Finally, the level of several JNK/c-Jun apoptosis pathway-related proteins were measured to characterize the mechanism of apoptosis. Results Our results showed that the proliferation rate was decreased and the apoptosis rate was increased in shCOPB2-treated RKO and HCT116 cells compared to those in controls. After the silencing of COPB2, JNK/c-Jun signal pathway activation was increased, the expression levels of apoptosis pathway-related proteins, such as Bad, p53 and Caspase 3, were also increased. Conclusion COPB2 gene silencing can inhibit RKO and HCT116 cells proliferation and induce apoptosis via the JNK/c-Jun signaling pathway.

scholarly journals Midkine Ameliorates the LPS-Induced Apoptosis of Airway Smooth Muscle Cells Through the Notch2 Pathway

2021 ◽  
Author(s):  
Huang Qifeng ◽  
Deng Tang ◽  
Li Lihua ◽  
Qian Jin ◽  
Li Qi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Signaling Pathway ◽  
Airway Smooth Muscle ◽  
Airway Remodeling ◽  
Muscle Cells ◽  
Cell Counting ◽  
Airway Smooth Muscle Cells ◽  
Extracellular Matrix Components ◽  
Proliferation And Apoptosis

Abstract Background: Airway smooth muscle cells (ASMCs) produce several cytokines during inflammation, causing changes in extracellular matrix components, leading to airway remodeling. Midkine (MK) promotes the chemotaxis of inflammatory cells and releases proinflammatory factors. Whether Notch and Midkine jointly affect the proliferation and apoptosis of ASMCs is unknown. This research aimed to study the role of MK in ASMCs using an LPS-induced acute lung injury model.Methods: ASMCs were cultured in vitro and divided into five groups according to treatment: control, lipopolysaccharide (LPS), non-target siRNA, MK siRNA, and g-secretase inhibitor LY411575. Cell proliferation was assessed using the Cell Counting Kit-8 assay. Apoptosis was measured by flow cytometry. Changes in the levels of cytokines related to the MK/Notch2 signaling pathway were detected by Western blotting, qPCR, and immunofluorescence.Results: LPS increased the mRNA and protein expression of MK and Notch2. MK silencing and LY411575 reduced this effect. LPS reduced the viability and increased the rate of apoptosis of ASMCs. This effect was attenuated by exogenous MK and enhanced by MK silencing and LY411575 treatment.Conclusions: The MK/Notch2 signaling pathway plays a regulatory role in ASMC proliferation and apoptosis in airway inflammation.

scholarly journals FOXH1 promotes lung cancer progression by activating the Wnt/β-catenin signaling pathway

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jun Zhang ◽  
Xian Zhang ◽  
Shasha Yang ◽  
Yanqiu Bao ◽  
Dongyuan Xu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Lung Cancer Cells ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Mesenchymal Transition

Abstract Background The expression of forkhead box protein H1 (FOXH1) is frequently upregulated in various cancers. However, the molecular mechanisms underlying the association between FOXH1 expression and lung cancer progression still remain poorly understood. Thus, the main objective of this study is to explore the role of FOXH1 in lung cancer. Methods The Cancer Genome Atlas dataset was used to investigate FOXH1 expression in lung cancer tissues, and the Kaplan–Meier plotter dataset was used to determine the role of FOXH1 in patient prognosis. A549 and PC9 cells were transfected with short hairpin RNA targeting FOXH1 mRNA. The Cell Counting Kit-8, colony formation, soft agar, wound healing, transwell invasion and flow cytometry assays were performed to evaluate proliferation, migration and invasion of lung cancer cells. Tumorigenicity was examined in a BALB/c nude mice model. Western blot analysis was performed to assess the molecular mechanisms, and β-catenin activity was measured by a luciferase reporter system assay. Results Higher expression level of FOXH1 was observed in tumor tissue than in normal tissue, and this was associated with poor overall survival. Knockdown of FOXH1 significantly inhibited lung cancer cell proliferation, migration, invasion, and cycle. In addition, the mouse xenograft model showed that knockdown of FOXH1 suppressed tumor growth in vivo. Further experiments revealed that FOXH1 depletion inhibited the epithelial-mesenchymal transition of lung cancer cells by downregulating the expression of mesenchymal markers (Snail, Slug, matrix metalloproteinase-2, N-cadherin, and Vimentin) and upregulating the expression of an epithelial marker (E-cadherin). Moreover, knockdown of FOXH1 significantly downregulated the activity of β-catenin and its downstream targets, p-GSK-3β and cyclin D1. Conclusion FOXH1 exerts oncogenic functions in lung cancer through regulation of the Wnt/β-catenin signaling pathway. FOXH1 might be a potential therapeutic target for patients with certain types of lung cancer.

scholarly journals LINC01152 upregulates MAML2 expression to modulate the progression of glioblastoma multiforme via Notch signaling pathway

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jianheng Wu ◽  
Nannan Wang ◽  
Ying Yang ◽  
Guangyuan Jiang ◽  
Qingchun Mu ◽  
...  
Keyword(s):  
Glioblastoma Multiforme ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Notch Signaling Pathway ◽  
Luciferase Reporter ◽  
Pcr Analysis ◽  
Psychological Pain ◽  
Protein Coding ◽  
Proliferation And Apoptosis ◽  
And Function

AbstractGlioblastoma multiforme (GBM) brings serious physical and psychological pain to GBM patients, whose survival rate remains not optimistic. Long noncoding RNAs (lncRNAs) have been reported to participate in the progression of many cancers, including GBM. However, the mechanism and function of long intergenic non-protein coding RNA 1152 (LINC01152) in GBM are still unclear. In our study, we aimed to explore the function and mechanism of LINC01152 in GBM. Then qRT-PCR analysis was implemented to search the expression of RNAs in GBM tissues and cells. Functional assays such as EdU assay, colony formation assay, TUNEL assay and flow cytometry analysis were conducted to estimate GBM cell proliferation and apoptosis. RNA pull down assay, luciferase reporter assay, RIP and ChIP assays were implemented to search the binding between molecules. As a result, we discovered that LINC01152 was upregulated in GBM tissues and cells. LINC01152 and mastermind like transcriptional coactivator 2 (MAML2) could both play the oncogenic part in GBM. Moreover, LINC01152 positively regulated MAML2 in GBM by sponging miR-466 and recruiting SRSF1. In turn, RBPJ/MAML2 transcription complex was found to activate the transcription of LINC01152 in GBM cells. In conclusion, LINC01152 could upregulate the expression of MAML2 to promote tumorigenesis in GBM via Notch signaling pathway.

scholarly journals Genome-wide identification of ZmSnRK2 genes and functional analysis of ZmSnRK2.10 in ABA signaling pathway in maize (Zea mays L)

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Tiandan Long ◽  
Binjie Xu ◽  
Yufeng Hu ◽  
Yayun Wang ◽  
Changqing Mao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Expression Patterns ◽  
Functional Study ◽  
Pcr Analysis ◽  
Whole Genome ◽  
Aba Signaling ◽  
Genome Database ◽  
Wide Range ◽  
Duplication Events ◽  
Aba Insensitive

Abstract Background Phytohormone abscisic acid (ABA) is involved in the regulation of a wide range of biological processes. In Arabidopsis, it has been well-known that SnRK2s are the central components of the ABA signaling pathway that control the balance between plant growth and stress response, but the functions of ZmSnRK2 in maize are rarely reported. Therefore, the study of ZmSnRK2 is of great importance to understand the ABA signaling pathways in maize. Results In this study, 14 ZmSnRK2 genes were identified in the latest version of maize genome database. Phylogenetic analysis revealed that ZmSnRK2s are divided into three subclasses based on their diversity of C-terminal domains. The exon-intron structures, phylogenetic, synteny and collinearity analysis indicated that SnRK2s, especially the subclass III of SnRK2, are evolutionally conserved in maize, rice and Arabidopsis. Subcellular localization showed that ZmSnRK2 proteins are localized in the nucleus and cytoplasm. The RNA-Seq datasets and qRT-PCR analysis showed that ZmSnRK2 genes exhibit spatial and temporal expression patterns during the growth and development of different maize tissues, and the transcript levels of some ZmSnRK2 genes in kernel are significantly induced by ABA and sucrose treatment. In addition, we found that ZmSnRK2.10, which belongs to subclass III, is highly expressed in kernel and activated by ABA. Overexpression of ZmSnRK2.10 partially rescued the ABA-insensitive phenotype of snrk2.2/2.3 double and snrk2.2/2.3/2.6 triple mutants and led to delaying plant flowering in Arabidopsis. Conclusion The SnRK2 gene family exhibits a high evolutionary conservation and has expanded with whole-genome duplication events in plants. The ZmSnRK2s expanded in maize with whole-genome and segmental duplication, not tandem duplication. The expression pattern analysis of ZmSnRK2s in maize offers important information to study their functions. Study of the functions of ZmSnRK.10 in Arabidopsis suggests that the ABA-dependent members of SnRK2s are evolutionarily conserved in plants. Our study elucidated the structure and evolution of SnRK2 genes in plants and provided a basis for the functional study of ZmSnRK2s protein in maize.

scholarly journals Cinobufagin Enhances the Sensitivity of Cisplatin-Resistant Lung Cancer Cells to Chemotherapy by Inhibiting the PI3K/AKT and MAPK/ERK Pathways

2021 ◽  
Author(s):  
Guangxin Zhang ◽  
Xueshibojie Liu ◽  
Yicun Wang ◽  
Chengyan Jin ◽  
Zhengyang Lu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Chemotherapy Resistance ◽  
Lung Cancer Cells ◽  
Cell Counting ◽  
Pcr Analysis ◽  
Tunel Staining ◽  
Chemotherapy Drugs

Abstract Background: Lung cancer patients always develop serious chemotherapy resistance after long-term use of cisplatin (DDP) treatment. It has been demonstrated that combination of DDP with other chemotherapy drugs may significantly reduce drug resistance. Cinobufagin (CB) showed potent anti-tumor effect against lung cancer. However, the relevance of CB and DDP resistance in lung cancer remains unclear. This article will study the effects of CB on reversing lung cell resistance in vitro and in vivo. Materials and Methods: The cell viability was evaluated using the Cell Counting Kit 8 (CCK8) assay. The apoptosis was detected by flow cytometry analysis and TUNEL staining. The invasiveness was detected by Invasion assay. The mRNA and protein of apoptosis-related proteins, P-AKT, P-PI3K, P-MEK1/2, P-ERK1/2 and MRP1 were estimated by qRT-PCR analysis and western blot analysis, respectively. In vivo antitumor activities were investigated by subcutaneous xenograft assay. Results: The present study firstly demonstrated that the sensitivity of DDP in DDP-resistant A549 (A549/DDP) cells was enhanced when treatment with CB. Moreover, CB combined with DDP significantly weakened the proliferation and increased apoptosis of A549/DDP cells. In addition, the expression level of Bcl-2 was increased, whereas Bax and Caspase-3 were activated when A549/DDP cells were treated with both drugs. Moreover, after treatment with IGF1 (activator of PI3K/AKT) or PMA (activator of MAPK/ERK) and mixed drugs (CB+DDP), the expressions of P-AKT, P-PI3K, P-MEK1/2 and P-ERK1/2 were increased. Finally, the results of in vivo experiments showed that the combination of DDP and CB significantly reduced the growth of tumors derived from A549/DDP cells. Conclusions: In summary, the results of this study indicate that the combination of CB and DDP can be considered an effective strategy to increase the sensitivity of DDP-resistant lung cancer cells to DDP by inhibiting the PI3K/AKT and MAPK/ERK pathways.

scholarly journals Crosstalk of the Wnt/β-Catenin Signaling Pathway in the Induction of Apoptosis on Cancer Cells

2021 ◽  
Vol 14 (9) ◽  
pp. 871
Author(s):  
Cristina Trejo-Solis ◽  
Angel Escamilla-Ramirez ◽  
Dolores Jimenez-Farfan ◽  
Rosa Angelica Castillo-Rodriguez ◽  
Athenea Flores-Najera ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Malignant Tumors ◽  
Cell Renewal ◽  
Stem Cell Renewal ◽  
Wide Range ◽  
Proliferation And Apoptosis ◽  
Cellular Context ◽  
Available Information

The Wnt/β-catenin signaling pathway plays a major role in cell survival and proliferation, as well as in angiogenesis, migration, invasion, metastasis, and stem cell renewal in various cancer types. However, the modulation (either up- or downregulation) of this pathway can inhibit cell proliferation and apoptosis both through β-catenin-dependent and independent mechanisms, and by crosstalk with other signaling pathways in a wide range of malignant tumors. Existing studies have reported conflicting results, indicating that the Wnt signaling can have both oncogenic and tumor-suppressing roles, depending on the cellular context. This review summarizes the available information on the role of the Wnt/β-catenin pathway and its crosstalk with other signaling pathways in apoptosis induction in cancer cells and presents a modified dual-signal model for the function of β-catenin. Understanding the proapoptotic mechanisms induced by the Wnt/β-catenin pathway could open new therapeutic opportunities.

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