MiR-34a suppresses cell proliferation in laryngeal cancer by targeting Prominin 1

2021 ◽  
Author(s):  
Xianyang Luo ◽  
Aimin Chen ◽  
Yi Zhou ◽  
Binghuang Zhang ◽  
Yuanqin Jiang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Laryngeal Cancer

scholarly journals Upregulation of Long Noncoding RNA_GAS5 Suppresses Cell Proliferation and Metastasis in Laryngeal Cancer via Regulating PI3K/AKT/mTOR Signaling Pathway

2021 ◽  
Vol 20 ◽  
pp. 153303382199007
Author(s):  
Wenlin Liu ◽  
Jiandong Zhan ◽  
Rong Zhong ◽  
Rui Li ◽  
Xiaoli Sheng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Laryngeal Cancer ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Proliferation And Metastasis ◽  
Cancer Tissues ◽  
Lncrna Gas5

Background: Laryngeal cancer is one of the most common malignant tumors among head and neck cancers. Accumulating studies have indicated that long noncoding RNAs (lncRNAs) play an important role in laryngeal cancer occurrence and progression, however, the functional roles and relative regulatory mechanisms of lncRNA growth arrest-specific transcript 5 (GAS5) in laryngeal cancer progression remain unclear. Methods: The expression of lncRNA GAS5 in both laryngeal cancer tissues and cell lines was evaluated using quantitative reverse transcription-polymerase chain reaction (RT-qPCR) assay. The relationships between lncRNA GAS5 expression and clinical parameters were also analyzed. To determine the biological function of lncRNA GAS5, a lncRNA GAS5-specific plasmid was first transfected into laryngeal cancer cells using lentiviral technology. Cell counting kit-8 assay, flow cytometry, and Transwell assays were used to detect in vitro cell proliferation, apoptosis, cycle distribution, and metastasis abilities, respectively. Furthermore, in vivo cell growth experiments were also performed using nude mice. Additionally, western blotting was performed to identify the underlying regulatory mechanism. Results: In the current study, lncRNA GAS5 was downregulated in laryngeal cancer tissues and its low expression was closely associated with poor tumor differentiation, advanced TNM stage, lymph node metastasis, and shorter overall survival time. In addition, lncRNA GAS5 upregulation significantly inhibited laryngeal cancer cell proliferation both in vitro and in vivo. Moreover, in response to lncRNA GAS5 overexpression, more laryngeal cancer cells were arrested at the G2/M stage, accompanied by increased cell apoptosis rates and suppressed migration and invasion capacities. Mechanistically, our data showed that the overexpression of lncRNA GAS5 significantly regulated the PI3K/AKT/mTOR signaling pathway. Conclusion: LncRNA GAS5 might act as a suppressor gene during laryngeal cancer development, as it suppressed cell proliferation and metastasis by regulating the PI3K/AKT/mTOR signaling pathway; thus, lncRNA GAS5 is a promising therapeutic biomarker for the treatment of laryngeal cancer.

scholarly journals Lentivirus-delivered nemo-like kinase small interfering RNA inhibits laryngeal cancer cell proliferation in vitro

2015 ◽  
Vol 12 (4) ◽  
pp. 5619-5624
Author(s):  
JUN TAI ◽  
YUANSHENG RAO ◽  
JUGAO FANG ◽  
ZHIGANG HUANG ◽  
ZHENKUN YU ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cancer Cell ◽  
Laryngeal Cancer ◽  
Small Interfering Rna ◽  
Cancer Cell Proliferation ◽  
Interfering Rna ◽  
Proliferation In Vitro

Enhanced apoptosis correlates with poor survival in patients with laryngeal cancer but not with cell proliferation, bcl-2 or p53 expression

1999 ◽  
Vol 35 (2) ◽  
pp. 231-237 ◽  
Author(s):  
P. Hirvikoski ◽  
E. Kumpulainen ◽  
J. Virtaniemi ◽  
R. Pirinen ◽  
L. Salmi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Laryngeal Cancer ◽  
Poor Survival ◽  
P53 Expression

scholarly journals Correlation of survivin, p53 and Ki-67 in laryngeal cancer Hep-2 cell proliferation and invasion

2015 ◽  
Vol 8 (8) ◽  
pp. 636-642 ◽  
Author(s):  
Shi-Geng Pei ◽  
Ju-Xiang Wang ◽  
Xue-Ling Wang ◽  
Qing-Jun Zhang ◽  
Hong Zhang
Keyword(s):  
Cell Proliferation ◽  
Laryngeal Cancer ◽  
Ki 67 ◽  
Proliferation And Invasion

scholarly journals Radiosensitization effect of hsa-miR-138-2-3p on human laryngeal cancer stem cells

PeerJ ◽  
2017 ◽  
Vol 5 ◽  
pp. e3233 ◽  
Author(s):  
Ying Zhu ◽  
Li-Yun Shi ◽  
Yan-Min Lei ◽  
Yan-Hong Bao ◽  
Zhao-Yang Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Cell Proliferation ◽  
Cancer Stem Cells ◽  
Cell Cycle Arrest ◽  
Laryngeal Cancer ◽  
Signal Pathway ◽  
Cycle Arrest ◽  
Anti Cancer ◽  
Radio Sensitivity

BackgroundTreatments that target cancer stem cells play an important role in the controlling and eliminating of tumor initiation as well as in development, progression, and chemotherapy/radiotherapy resistance. In our previous study, we cultured and harvested human laryngeal cancer stem cells (CSCs) and applied microRNA biochips to screen differentially expressed miRNAs that were related to radiation tolerance in irradiated human laryngeal CSCs. According to the predicted genes and pathways of differential miRNAs target, down-regulated expression of hsa-miR-138-2-3p under radiation was thought to play a key role in enhancing the radio-sensitivity in human laryngeal squamous cancer stem cells.MethodTo investigate the radiational enhancement of hsa-miR-138-2-3p, we transfected hsa-miR-138-2-3p mimics that were synthesized based on the sequences of hsa-miR-138-2-3pin vitrointo human laryngeal CSCs (Hep-2, M2e, and TU212 cell lines) to make hsa-miR-138-2-3p overexpressed, and the tumorous specialities of CSCs, like cell proliferation, invasion, apoptosis, cell cycle arrest, and DNA damage were evaluated by CCK-8 assay, clone formation assay, invasion assay, flow cytometry, and comet assay. Furthermore, we explored the signal transduction pathways that regulated the cancer stem cell initiation, development, invasion, apoptosis and cell cycle arrest, which were controlled by hsa-miR-138-2-3p.ResultOverexpressed hsa-miR-138-2-3p played a key role in many anti-cancer biological processes in human laryngeal CSCs: (1) it decreased laryngeal CSCs proliferation and invasion in response to radiotherapy; (2) it increased the proportion of early and late apoptosis in laryngeal CSCs after radiation, raised G1 phase arrest in laryngeal CSCs after radiation, and decreased the proportion of S stage cells of cell cycle that were related to radio-resistance in laryngeal CSCs; (3) it down-regulated the expression of β-catenin in Wnt signal pathway that was related to the tolerance of laryngeal CSCs to radiotherapy; (4) it down-regulated the expression of YAP1 in Hippo signal pathway that regulated cell proliferation, invasion and apoptosis; (5) it up-regulated the expression of p38 and JNK1 in MAPK signal pathway that was concerned to radio-sensitivity.ConclusionIn the present study, it was found that hsa-miR-138-2-3p regulated the Wnt/β-catenin pathways, the Hippo/YAP1 pathways, and the MAPK/p38/JNK1 pathways that were involved in cell proliferation, invasion, apoptosis, cell cycle arrest, radio-resistance and radio-sensitivity in laryngeal CSCs. These results will be useful for a better understanding of the cell biology of hsa-miR-138-2-3p in laryngeal CSCs, and for serving hsa-miR-138-2-3p as a promising biomarker and as a target for diagnosis and for novel anti-cancer therapies for laryngeal cancers.

LncRNA DUXAP8 promotes the progression of laryngeal cancer through targeting miR-384/ POU2F1 axis

2020 ◽  
Author(s):  
Zhanfeng Yan ◽  
Xiaohui Wen ◽  
Jinsheng Dai ◽  
Jinfeng Liu ◽  
Pengpeng Hao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Laryngeal Cancer ◽  
Tumor Model ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Normal Tissues ◽  
Tumor Tissues ◽  
High Level

Abstract Background Laryngeal cancer is the highest incidence of head and neck cancers in the world. Increasing evidences have demonstrated that long non-coding RNAs (lncRNAs) play crucial roles in the progression of laryngeal cancer. Despite of the essential role of lncRNA DUXAP8 in many human cancers, its function and specific mechanisms in laryngeal cancer are poorly understood. Methods Differentially expression analysis of lncRNAs in GSE59652 dataset was performed by using limma package of R language. The expression of DUXAP8, miR-384 and candidate mRNAs was evaluated by qRT-PCR. Luciferase reporter assay and RIP assay were performed to determine the direct correlation between DUXAP8, miR-384 and POU2F1. Cell proliferation of laryngeal cancer cell lines TU212 and TU177 cells was evaluated by using CCK-8 assay, colony formation assay and EdU staining assay. Xenograft tumor model in vivo and rescue experiments were performed to explore the function and mechanisms of DUXAP8 in laryngeal cancer. Results The expression of DUXAP8 in tumor tissues was higher than that in adjacent normal tissues. High level of DUXAP8 was closely correlated to the worse prognosis of laryngeal cancer patients. Knockdown of DUXAP8 inhibited the proliferation of TU212 and TU177 cells in vitro, as well as tumor growth in vivo. Furthermore, overexpression of POU2F1 significantly attenuated the inhibitory effect of sh-DUXAP8 on cell proliferation of TU212 and TU177 cells. In addition, sh-DUXAP8 significantly decreased the expression of DUXAP8 and POU2F1, while increased miR-384 expression in tumor tissues compared with sh-NC group. Conclusion DUXAP8 acted as a sponge of tumor suppressor miR-384 and then upregulated POU2F1 expression, thereby promoted the development of laryngeal cancer. Our findings suggest that DUXAP8 may serve as a potential therapeutic target for laryngeal cancer.

scholarly journals Curcumin inhibits cell proliferation and promotes apoptosis of laryngeal cancer cells through Bcl-2 and PI3K/Akt, and by upregulating miR-15a

2017 ◽  
Vol 14 (4) ◽  
pp. 4937-4942 ◽  
Author(s):  
Shaofeng Mou ◽  
Zhongxin Zhou ◽  
Yukai He ◽  
Fuxing Liu ◽  
Lili Gong
Keyword(s):  
Cell Proliferation ◽  
Cancer Cells ◽  
Laryngeal Cancer
Sign in / Sign up

Export Citation Format

Share Document