scholarly journals Effect of Notch1 Signaling on Cellular Proliferation and Apoptosis of Human Laryngeal Carcinoma

2021 ◽  
Author(s):  
Dawei Li ◽  
Yifei Zhang ◽  
Penghui Chen ◽  
Jin Xie ◽  
Dan Xu
Keyword(s):  
Cell Proliferation ◽  
Cancer Cells ◽  
Laryngeal Cancer ◽  
Cell Apoptosis ◽  
Laryngeal Carcinoma ◽  
Apoptosis Resistance ◽  
Neoplastic Cells ◽  
Notch1 Signaling ◽  
Proliferation And Apoptosis ◽  
Signaling Activity

Abstract The pathological processes of occurrence and development of malignancies include the excessive proliferation and apoptosis resistance of neoplastic cells. The study aims to identify the effects of Notch1 signaling on the proliferation and apoptosis of laryngeal cancer cells in hypoxic microenvironment. Notch1 and Ki-67 expression in laryngeal squamous cell carcinoma (LSCC) tissue samples were detected by immunohistochemistry. The apoptotic index (AI) of LSCC was evaluated by TUNEL method. In laryngeal cancer cells, small interfering RNA (siRNA) technology was to inhibit Notch1 expression. Meanwhile, Real-time PCR detected Notch1, Hes1 and Hey1 mRNA expression, and Western blot detected Notch1 and Notch1 intracellular domain (N1ICD) protein expression. Annexin V-FITC/propidium iodide staining and Cell Counting Kit‑8 methods measured cell apoptosis and proliferation, respectively. Notch1 expression was detected in 63.55％(68/107) of LSCC samples and was significantly related to the proliferation index (PI) (P < 0.05) and AI (P < 0.05) in LSCC tissues. Furthermore, it was confirmed that hypoxia could induce proliferation and inhibit apoptosis of laryngeal carcinoma cells (P < 0.05). Meanwhile, Notch1 expression and Notch1 signaling activity could be upregulated by hypoxia (P < 0.05). In contrast, suppression of Notch1 signaling activity in hypoxic neoplastic cells could obviously decrease cell proliferation and increase cell apoptosis (both P<0.05). Our study has demonstrated that hypoxia may promote cell proliferation and inhibit cell apoptosis of laryngeal carcinoma. Notch1 signalling may exert a pivotal role in regulating the proliferation and apoptosis resistance of laryngeal cancer cells under hypoxia.

scholarly journals Notch1 Signaling Modulates Hypoxia-induced Multidrug Resistance of Human Laryngeal Cancer Cells

2021 ◽  
Author(s):  
Dawei Li ◽  
Dan Xu ◽  
Penghui Chen ◽  
Jin Xie
Keyword(s):  
Multidrug Resistance ◽  
Cancer Cells ◽  
Laryngeal Cancer ◽  
Laryngeal Carcinoma ◽  
Drug Transport ◽  
Malignant Tumors ◽  
Carcinoma Cells ◽  
Cell Counting ◽  
Apoptosis Resistance ◽  
Notch1 Signaling

Abstract Background: Laryngeal carcinoma is one of the common malignant tumors of the head and neck. Multidrug resistance (MDR) remains a critical problem in the chemotherapy for patients with laryngeal cancer. This study aims to clarify the role and mechanisms of Notch1 signaling on MDR induced by hypoxia in laryngeal cancer cells.Methods and Results: Laryngeal carcinoma cells were cultured under normoxia or hypoxia. Notch1 expression was inhibited by small interfering RNA (siRNA). The expression of Notch1, Hes1, Hey1, MDR1 and survivin mRNA was determined by Real-time PCR. The expression of Notch1, Notch1 intracellular domain (N1ICD), MDR1/P-gp and survivin protein was detected by Western blot. Current research showed that hypoxia could upregulate Notch1 expression and the activity of Notch1 signaling. Furthermore, suppression of Notch1 expression could effectively down-regulate the activity of Notch1 signaling and the expression of MDR and survivin genes in laryngeal cancer cells under hypoxia (P<0.05). Cell Counting Kit-8 (CCK-8) assay confirmed that the sensitivity of hypoxic laryngeal cancer cells to a variety of drugs could be up-regulated by suppressing Notch1 expression (P<0.05). Additionally, flow cytometry (FCM) showed that suppression of Notch1 expression significantly increased cisplatin-induced apoptosis and intracellular Rh123 (Rh123) accumulation in hypoxic laryngeal carcinoma cells (P<0.05). Conclusions: Notch1 signalling could be regarded as a pivotal regulator for mediating hypoxia-induced MDR in laryngeal cancer cells by regulating survivin-mediated apoptosis resistance and MDR1/P-gp-mediated drug transport.

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 Upregulation of Circular RNA Itchy E3 Ubiquitin Protein Ligase Inhibits Cell Proliferation and Promotes Cell Apoptosis Through Targeting MiR-197 in Prostate Cancer

2019 ◽  
Vol 18 ◽  
pp. 153303381988686 ◽  
Author(s):  
Yuan Yuan ◽  
Xiaogang Chen ◽  
Enying Huang
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Western Blot ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Circular Rna ◽  
Micro Rna ◽  
Prostate Cancer Cells ◽  
Ubiquitin Protein Ligase ◽  
Proliferation And Apoptosis

Objective: This study aimed to investigate the effect of circular RNA itchy E3 ubiquitin protein ligase on cell proliferation and apoptosis and to explore its target micro-RNAs in prostate cancer cells. Methods: Circular RNA itchy E3 ubiquitin protein ligase expression in human prostate cancer cells and normal prostate epithelial cells was determined by real time-quantitative polymerase chain reaction assay. Circular RNA itchy E3 ubiquitin protein ligase overexpression plasmids (circular RNA itchy E3 ubiquitin protein ligase(+) group and control overexpression plasmids group were transfected with PC-3 cells. Rescue experiment was performed by transfection of circular RNA itchy E3 ubiquitin protein ligase overexpression and micro-197 overexpression plasmids (circular RNA itchy E3 ubiquitin protein ligase overexpression plasmids/micro RNA (+) group) into PC-3 cells. Cell Counting Kit-8 and annexin V/propidium iodide assays were conducted to evaluate cell proliferation and apoptosis, respectively. Western blot was performed to determine the expressions of apoptotic-related markers. Results: Circular RNA itchy E3 ubiquitin protein ligase expression was decreased in DU 145, 22RV1, VCaP, and PC-3 cells compared to RWPE cells. In PC-3 cells, cell proliferation rate was reduced in circular RNA itchy E3 ubiquitin protein ligase overexpression plasmids group compared to control overexpression plasmids group at 48 hours and 72 hours. Cell apoptosis rate was elevated in circular RNA itchy E3 ubiquitin protein ligase overexpression plasmids group compared to control overexpression plasmids group at 48 hours, and Western blot showed the similar results. Micro RNA-197 but not micro RNA-31 or micro RNA-432 was the target micro-RNA of circular RNA itchy E3 ubiquitin protein ligase. In rescue experiments, cell proliferation rate was elevated, but apoptosis rate was reduced in circular RNA itchy E3 ubiquitin protein ligase overexpression plasmids/micro RNA (+) group compared to circular RNA itchy E3 ubiquitin protein ligase overexpression plasmids group, indicating that circular RNA itchy E3 ubiquitin protein ligase upregulation inhibited cell proliferation but promoted apoptosis through downregulating micro RNA-197. Conclusion: Circular RNA itchy E3 ubiquitin protein ligase upregulation suppresses cell proliferation but promotes apoptosis through targeting micro RNA-197 in prostate cancer. Our study may provide a new insight for the treatment of prostate cancer.

Effect of Yes Associated Protein 1 Silence on Proliferation and Apoptosis of Bladder Cancer Cells

2021 ◽  
Vol 11 (5) ◽  
pp. 857-863
Author(s):  
Gaoliang Wu ◽  
Chao Hao ◽  
Xueliang Qi ◽  
Jianqiang Nie
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Direct Role ◽  
Cycle Arrest ◽  
Proliferation And Apoptosis ◽  
Bladder Cancer Cells ◽  
Cancer Tissues

Yes Associated Protein 1 (YAP) can act as either an oncoprotein or a tumor suppressor in different cellular contexts. However, the reports about the direct role of YAP silence in bladder cancer cells are rare. We designed loss-off-function experiments to investigate the effect of YAP knockdown on bladder cancer cell proliferation, cell cycle and cell apoptosis. We examined YAP expression in human bladder cancer and paracancerous tissues using RT-qPCR, western blot and immunohisto-chemistry. YAP short hairpin RNA (shRNA) was successfully constructed and transfected into T24 cells to knockdown YAP. Cell proliferation, cell cycle and cell apoptosis were analyzed by CCK-8 and flow cytometry. We found the expression levels of YAP mRNA and protein were significantly increased in the bladder cancer tissues when compared with that in the paracancerous tissues. shRNA YAP inhibited cell proliferation, induced cell cycle arrest at G1 phase, and induced cell apoptosis. In conclusion, our findings provided the first evidence that YAP knockdown could inhibit cell proliferation and induce cell apoptosis of bladder cancer cells. YAP inhibition may be beneficial in the treatment of bladder cancer.

Effects of miR-21 Mediating Nerve Cell Adhesion Molecule (NCAM) and Glial Cell-Line Derived Neurotrophic Factor (GDNF) Signals on the Proliferation and Apoptosis of Lung Cancer Cells

2021 ◽  
Vol 11 (9) ◽  
pp. 1769-1773
Author(s):  
Dongliang Li ◽  
Chaoqun Dong ◽  
Zejun Fu ◽  
Yongming Song
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cell Adhesion ◽  
Cancer Cells ◽  
Cell Line ◽  
Adhesion Molecule ◽  
Neurotrophic Factor ◽  
Cell Apoptosis ◽  
Cell Adhesion Molecule ◽  
Proliferation And Apoptosis

Our study assessed the effect of miR-21 mediating Nerve Cell Adhesion Molecule (NCAM) and Glial Cell-line Derived Neurotrophic Factor (GDNF) on the proliferation and apoptosis of lung cancer cells. Lung cancer cell-line H460 cells were grouped as Lung cancer group (LC group) (normal cultivation); Mimic group (SI group) which was transfected with 120 nmol/L miR-21 mimics and liposomes; Inhibitor group (IN group) (transfection of miR-21 inhibitor and liposomes) followed by analysis of cell apoptosis by Hoechst 33258 staining, GDNF level by immunohistochemistry, miR-21 level by qRT-PCR, cell proliferation by CCK-8 and NCAM level by western blot. miR-21 content was significantly increased in SI group, indicating a successful transfection. The nucleus shrinkage rate in IN group and LC group was higher than SI group (P <0.05) and IN group had highest number of apoptotic cells, lowest cell proliferation and NCAM level among three groups (P <0.05). SI group showed significantly higher positive GDNF staining than IN and LC group (both P <0.05). miR-21 promotes H460 cell proliferation and inhibits cell apoptosis by upregulating NCAM and GDNF.

MiR-203 Mimic Down-Regulates Baculoviral IAP Repeat Containing 5 Expression and Affects Proliferation and Apoptosis of Gastric Cancer Cells

2020 ◽  
Vol 10 (1) ◽  
pp. 81-86
Author(s):  
Yanhua Xu ◽  
Pailan Peng ◽  
Qiuyuan Zhou
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Real Time Pcr ◽  
Cell Apoptosis ◽  
Bioinformatics Analysis ◽  
Gastric Cancer Cells ◽  
Tumor Tissues ◽  
Proliferation And Apoptosis ◽  
Cancer Bioinformatics

Human baculovirus IAP repeats containing protein 5 (BIRC5) is the most inhibitor of cell apoptosis. Abnormal miR-203 level is associated with the pathogenesis of gastric cancer. Bioinformatics analysis revealed a relationship between miR-203 and BIRC5. Our study assessed miR-203’s role in gastric cancer cells. Tumor tissues and adjacent tissues were collected. miR-203 and BIRC5 mRNA expression in SGC7901 and MKN45 cells was detected by real-time PCR. SGC7901 cells were divided into miR-NC group and miR-203 mimic group followed by analysis of cell proliferation by EdU staining. Compared to adjacent tissues, miR-203 level was decreased and BIRC5 was increased. There was a targeted relationship between miR-203 and BIRC5. Compared with RGM- 1 cells, miR-203 in SGC7901 and MKN45 cells was significantly downregulated and BIRC5 was upregulated. miR-203 mimic significantly downregulated BIRC5 in SGC7901 cells, promoted cell apoptosis, and attenuated cell proliferation. Decreased miR-203 expression and increased BIRC5 expression is associated with the pathogenesis of gastric cancer. MiR-203 can inhibit the expression of BIRC5, inhibit proliferation of gastric cancer cells and induce apoptosis.

scholarly journals LncRNA UCA1 promotes development of gastric cancer via the miR-145/MYO6 axis

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
An Yang ◽  
Xin Liu ◽  
Ping Liu ◽  
Yunzhang Feng ◽  
Hongbo Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Cell Lines ◽  
Development Of Gastric Cancer

Abstract Background Long noncoding RNA (lncRNA), urothelial carcinoma-associated 1 (UCA1) is aberrantly expressed in multiple cancers and has been verified as an oncogene. However, the underlying mechanism of UCA1 in the development of gastric cancer is not fully understood. In the present study, we aimed to identify how UCA1 promotes gastric cancer development. Methods The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) data were used to analyze UCA1 and myosin VI (MYO6) expression in gastric cancer. Western blot and quantitative real-time PCR (QPCR) were performed to test the expression level of the UCA1/miR-145/MYO6 axis in gastric cancer cell lines and tissues. The roles of the UCA1/miR-145/MYO6 axis in gastric cancer in vitro and in vivo were investigated by CCK-8 assay, flow cytometry, siRNAs, immunohistochemistry, and a mouse xenograft model. The targeted relationship among UCA1, miR-145, and MYO6 was predicted using LncBase Predicted v.2 and TargetScan online software, and then verified by luciferase activity assay and RNA immunoprecipitation. Results UCA1 expression was higher but miR-145 expression was lower in gastric cancer cell lines or tissues, compared to the adjacent normal cell line or normal tissues. Function analysis verified that UCA1 promoted cell proliferation and inhibited cell apoptosis in the gastric cancer cells in vitro and in vivo. Mechanistically, UCA1 could bind directly to miR-145, and MYO6 was found to be a downstream target gene of miR-145. miR-145 mimics or MYO6 siRNAs could partly reverse the effect of UCA1 on gastric cancer cells. Conclusions UCA1 accelerated cell proliferation and inhibited cell apoptosis through sponging miR-145 to upregulate MYO6 expression in gastric cancer, indicating that the UCA1/miR-145/MYO6 axis may serve as a potential therapeutic target for gastric cancer.

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.

ILF3-AS1 promotes cell proliferation and inhibits cell apoptosis of breast cancer by binding with miR-4429 to upregulate RAB14

2021 ◽  
pp. 096032712198942
Author(s):  
Xiaoxue Zhang ◽  
Xianxin Xie ◽  
Kuiran Gao ◽  
Xiaoming Wu ◽  
Yanwei Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Breast Cancer Cell ◽  
Cell Apoptosis ◽  
Breast Cancer Cells ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Cancer Tissues

As one of the leading causes of cancer-related deaths among women, breast cancer accounts for a 30% increase of incidence worldwide since 1970s. Recently, increasing studies have revealed that the long non-coding RNA ILF3-AS1 is involved in the progression of various cancers. Nevertheless, the role of ILF3-AS1 in breast cancer remains largely unknown. In the present study, we found that ILF3-AS1 was highly expressed in breast cancer tissues and cells. ILF3-AS1 silencing inhibited breast cancer cell proliferation, migration and invasion, and promoted cell apoptosis. ILF3-AS1 bound with miR-4429 in breast cancer cells. Moreover, RAB14 was a downstream target of miR-4429, and miR-4429 expression was negatively correlated with RAB14 or ILF3-AS1 expression in breast cancer tissues. The result of rescue experiments demonstrated that overexpression of RAB14 can reverse the inhibitory effect of ILF3-AS1 knockdown on breast cancer cell proliferation, migration and invasion. Overall, ILF3-AS1 promotes the malignant phenotypes of breast cancer cells by interacting with miR-4429 to regulate RAB14, which might offer a new insight into the underlying mechanism of breast cancer.

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