scholarly journals FGF16 regulated by miR-520b enhances the cell proliferation of lung cancer

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 419-427
Author(s):  
Wenfeng He ◽  
Xia Liu ◽  
Zhijie Luo ◽  
Longmei Li ◽  
Xisheng Fang
Keyword(s):  
Lung Cancer ◽  
Cancer Progression ◽  
Untranslated Region ◽  
Target Gene ◽  
Regulatory Mechanism ◽  
The Novel ◽  
Accelerated Growth ◽  
High Level ◽  
Cancer Tissues ◽  
Great Damage

Abstract FGF16 is implicated in the progression of some specific types of cancers, such as embryonic carcinoma, ovarian cancer, and liver cancer. Yet, the function of FGF16 in the development of lung cancer remains largely unexplored. In this study, we present the novel function of FGF16 and the regulation of miR-520b on FGF16 in lung cancer progression. In clinical lung cancer tissues, FGF16 is overexpressed and its high level is negatively associated with the low level of miR-520b. Furthermore, both the transcription and translation levels of FGF16 are restrained by miR-520b in lung cancer cells. For the regulatory mechanism investigation, miR-520b is able to directly bind to the 3′-untranslated region (3′UTR) of FGF16 mRNA, leading to its mRNA cleavage in the cells. Functionally, miR-520b reduces the growth of lung cancer and its inhibitor anti-miR520b is able to promote the growth through competing endogenous miR-520b. Moreover, FGF16 silence using RNA interference is capable of doing great damage to anti-miR-520b-accelerated growth of lung cancer. Thus, our finding indicates that FGF16 is a new target gene of miR-520b in lung cancer. For lung cancer, FGF16 may serve as a novel biomarker and miR-520b/FGF16 may be useful in clinical treatment.

scholarly journals POU2F2 promotes the proliferation and motility of lung cancer cells by activating AGO1

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ronggang Luo ◽  
Yi Zhuo ◽  
Quan Du ◽  
Rendong Xiao
Keyword(s):  
Lung Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Cancer Tissues

Abstract Background To detect and investigate the expression of POU domain class 2 transcription factor 2 (POU2F2) in human lung cancer tissues, its role in lung cancer progression, and the potential mechanisms. Methods Immunohistochemical (IHC) assays were conducted to assess the expression of POU2F2 in human lung cancer tissues. Immunoblot assays were performed to assess the expression levels of POU2F2 in human lung cancer tissues and cell lines. CCK-8, colony formation, and transwell-migration/invasion assays were conducted to detect the effects of POU2F2 and AGO1 on the proliferaion and motility of A549 and H1299 cells in vitro. CHIP and luciferase assays were performed for the mechanism study. A tumor xenotransplantation model was used to detect the effects of POU2F2 on tumor growth in vivo. Results We found POU2F2 was highly expressed in human lung cancer tissues and cell lines, and associated with the lung cancer patients’ prognosis and clinical features. POU2F2 promoted the proliferation, and motility of lung cancer cells via targeting AGO1 in vitro. Additionally, POU2F2 promoted tumor growth of lung cancer cells via AGO1 in vivo. Conclusion We found POU2F2 was highly expressed in lung cancer cells and confirmed the involvement of POU2F2 in lung cancer progression, and thought POU2F2 could act as a potential therapeutic target for lung cancer.

scholarly journals The Role of Cavin3 in the Progression of Lung Cancer and Its Mechanism

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Gaozhong Sun ◽  
Kewei Ni
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Tumor Formation ◽  
Migration And Invasion ◽  
Clinical Value ◽  
Promote Cell Proliferation ◽  
Cancer Tissues

Objective. The purpose of this study was to describe the role of Cavin3 in the progression of lung cancer and its underlying mechanism. Methods. Totally, 200 cases of lung cancer tissues and corresponding paracancer tissues were collected. Cavin3 expression in samples was determined by qRT-PCR, and the correlation with lung cancer stages as well as prognosis was statistically analyzed combined with matched clinical information. To investigate the mechanism of Cavin3 in lung cancer progression, firstly, Cavin3 was detected in lung cancer cell lines A549, PC9, and H520. Then, cells with stable Cavin3 overexpression and Cavin3 knockout were established to determine the effect of Cavin3 overexpression on the mammalian target of rapamycin (mTOR) signaling pathway. Subsequently, cells were harvested for cell proliferation, migration, and invasion assays in vitro, as well as nude mouse transplantation tumor experiment in vivo. Results. Cavin3 was seen to be highly expressed in cancer tissues. Statistical analysis with matched clinical data showed that Cavin3 as a prognostic indicator of lung cancer had important clinical value. In addition, it could be found that high expression of Cavin3 was able to promote cell proliferation, migration, and invasion and also potentiate tumor formation in vivo. Conclusion. Cavin3 was highly expressed in lung cancer, and it was capable to promote cell proliferation, invasion, and migration.

scholarly journals miR-195-5p Suppresses Lung Cancer Cell Proliferation, Migration, and Invasion Via FOXK1

2020 ◽  
Vol 19 ◽  
pp. 153303382092258 ◽  
Author(s):  
Zhiqiang Long ◽  
Yadong Wang
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Migration And Invasion ◽  
Lung Cancer Cell ◽  
Forkhead Box ◽  
Enhanced Expression ◽  
Proliferation And Metastasis ◽  
Cancer Tissues

Lung cancer remains one of the leading causes of cancer deaths around the world. Previous studies have shown that microRNAs have pivotal functions in tumorigenesis including lung cancer. It is reported that microRNA-195-5p acts as a tumor suppressor role in human cancers. However, the function and molecular mechanism of microRNA-195-5p in lung cancer progression is still unclear. In the present study, the results showed that the expression of microRNA-195-5p was downregulated both in lung cancer tissues and in lung cancer cell lines. Enhanced expression of microRNA-195-5p inhibited cell proliferation, migration, and invasion in lung cancer cells. Furthermore, Forkhead box k1 was identified as the direct target of microRNA-195-5p. Forkhead box k1 overexpression could restore the repressed cell proliferation and metastasis caused by microRNA-195-5p overexpression. Our results demonstrated that a functional mechanism of microRNA-195-5p in regulating lung cancer. It indicates that microRNA-195-5p may regulate lung cancer growth and metastasis through the regulation of Forkhead box k1, highlighting the potential application for the treatment of lung cancer in the future.

LncRNA HOXA-AS2 Facilitates Cervical Cancer Progression and Angiogenesis via miR-509-3p/BTN3A1 Axis

2020 ◽  
Author(s):  
Ruxiang Chen ◽  
Ping He
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Regulatory Mechanism ◽  
Tube Formation ◽  
Biological Role ◽  
Luciferase Reporter ◽  
Inhibitory Influence ◽  
Proliferation And Metastasis ◽  
Cancer Tissues

Abstract Background: Cervical cancer, the leading cause of cancer-relevant mortality in females, is an aggressive malignant tumor. Tumor angiogenesis is vital for cell proliferation and metastasis in cancers. Accumulating studies have claimed that long non-coding RNAs (lncRNAs) participate in the progression of various cancers. The aim of this research is to explore the biological role and regulatory mechanism of LncRNA HOXA-AS2 in cervical cancer.Methods: Experiments including RT-qPCR, western blot, RIP, MTT, EdU, transwell, luciferase reporter, RIP, FISH, tube formation assays were applied to investigate the biological role and regulatory mechanism of LncRNA HOXA-AS2 in cervical cancer.Results: In current study, the results disclosed that HOXA-AS2 was notably upregulated in cervical cancer tissues and cell lines, and high HOXA-AS2 expression was strongly associated with poor prognosis of cervical cancer patients. Furthermore, HOXA-AS2 contributed to cell proliferation, migration, invasion and angiogenesis in cervical cancer. In addition, HOXA-AS2 absorbed miR-509-3p and miR-509-3p targeted BTN3A1 in cervical cancer. Besides, BTN3A1 overexpression partly rescued the inhibitory influence of HOXA-AS2 knockdown on cervical cancer progression and angiogenesis. Overall, HOXA-AS2 promoted cervical cancer progression and angiogenesis through sponging miR-509-3p to elevate BTN3A1 expression. Conclusions: In other words, this paper was the first to study the molecular regulatory mechanism of HOXA-AS2 in cervical cancer and certified that HOXA-AS2 accelerated progression and angiogenesis in cervical cancer by targeting miR-509-3p/BTN3A1 axis, which may become a beneficial therapeutic target for cervical cancer.

scholarly journals Circular RNA-ITCH Suppresses Lung Cancer Proliferation via Inhibiting the Wnt/β-Catenin Pathway

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Li Wan ◽  
Lin Zhang ◽  
Kai Fan ◽  
Zai-Xing Cheng ◽  
Quan-Chao Sun ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Progression ◽  
Ectopic Expression ◽  
Circular Rna ◽  
Circular Rnas ◽  
Parental Cancer ◽  
Cancer Proliferation ◽  
Mirna Sponge ◽  
Tumor Tissues ◽  
Cancer Tissues

As a special form of noncoding RNAs, circular RNAs (circRNAs) played important roles in regulating cancer progression mainly by functioning as miRNA sponge. While the function of circular RNA-ITCH (cir-ITCH) in lung cancer is still less reported, in this study, we firstly detected the expression ofcir-ITCHin tumor tissues and paired adjacent noncancer tissues of 78 patients with lung cancer using a TaqMan-based quantitative real-time PCR (qRT-PCR). The results showed that the expression ofcir-ITCHwas significantly decreased in lung cancer tissues. In cellular studies,cir-ITCHwas also enhanced in different lung cancer cell lines, A549 and NIC-H460. Ectopic expression ofcir-ITCHmarkedly elevated its parental cancer-suppressive gene, ITCH, expression and inhibited proliferation of lung cancer cells. Molecular analysis further revealed thatcir-ITCHacted as sponge of oncogenic miR-7 and miR-214 to enhance ITCH expression and thus suppressed the activation of Wnt/β-catenin signaling. Altogether, our results suggested thatcir-ITCHmay play an inhibitory role in lung cancer progression by enhancing its parental gene, ITCH, expression.

scholarly journals TNFAIP3 Suppresses Lung Cancer Progression via Regulating Cell Proliferation and Apoptosis

2020 ◽  
Author(s):  
Han Chen ◽  
Jie Gao ◽  
Yongsheng Yu ◽  
Qian Zhou ◽  
Shan yongqi
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Colony Formation ◽  
The Cancer Genome Atlas ◽  
Lung Cancer Cells ◽  
Protein Levels ◽  
Cancer Tissues

Abstract Background: The ubiquitin-editing enzyme TNF inducible protein 3 (TNFAIP3) is a crucial regulator of inflammation and immunity. It is also involved in tumorigenesis of various cancers such as lymphomas, colorectal tumors and breast cancer. In this study, we aimed to explore the role and regulatory mechanism of TNFAIP3 in lung cancer. Methods: The expression of TNFAIP3 was determined in the Cancer Genome Atlas (TCGA) database. The levels of TNFAIP3 in lung cancer tissues was determined by immunohistochemistry (IHC) assay. TNFAIP3 knockdown and overexpression were performed, followed by further evaluation of cell viability, cell cycle and apoptosis. Cell cycle and apoptosis were observed by using flow cytometry and the key regulatory proteins were detected by western blotting. Colony formation assessment and EdU assay were adopted to check cell proliferation. Results: TNFAIP3 expression was downregulated in lung cancer tissues at both mRNA and protein levels, comparing with that in adjacent non-tumor tissues. Consequently, the colony formation ability of lung cancer cells was enhanced, and the number of EdU positive lung cancer cells was increased. By contrast, elevated TNFAIP3 expression resulted in decreased colony formation ability of lung cancer cells. Mechanistically, TNFAIP3 overexpression rendered cell cycle of lung cancer cells halted at G0/G1 phase and caused apoptosis of lung cancer cells.Conclusion: Our data suggested that TNFAIP3 exhibits tumor suppressive roles in lung cancer.

scholarly journals High level of BRD4 promotes non-small cell lung cancer progression

Oncotarget ◽  
2016 ◽  
Vol 7 (8) ◽  
pp. 9491-9500 ◽  
Author(s):  
Yun-Fei Liao ◽  
Yong-Bing Wu ◽  
Xiang Long ◽  
Shu-Qiang Zhu ◽  
Chun Jin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Progression ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
High Level

scholarly journals Characterization of Glycolysis-Associated Molecules in the Tumor Microenvironment Revealed by Pan-Cancer Tissues and Lung Cancer Single Cell Data

Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1788
Author(s):  
Jinfen Wei ◽  
Kaitang Huang ◽  
Zixi Chen ◽  
Meiling Hu ◽  
Yunmeng Bai ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Progression ◽  
Single Cells ◽  
Gene Expression Signature ◽  
Human Lung Cancer ◽  
Driver Genes ◽  
Molecular Features ◽  
Cancer Types ◽  
Cancer Tissues ◽  
Pan Cancer

Altered metabolism is a hallmark of cancer and glycolysis is one of the important factors promoting tumor development. There is however still a lack of molecular characterization glycolysis and comprehensive studies related to tumor glycolysis in the pan-cancer landscape. Here, we applied a gene expression signature to quantify glycolysis in 9229 tumors across 25 cancer types and 7875 human lung cancer single cells and verified the robustness of signature using defined glycolysis samples from previous studies. We classified tumors and cells into glycolysis score-high and -low groups, demonstrated their prognostic associations, and identified genome and transcriptome molecular features associated with glycolysis activity. We observed that glycolysis score-high tumors were associated with worse prognosis across cancer types. High glycolysis tumors exhibited specific driver genes altered by copy number aberrations (CNAs) in most cancer types. Tricarboxylic acid (TCA) cycle, DNA replication, tumor proliferation and other cancer hallmarks were more active in glycolysis-high tumors. Glycolysis signature was strongly correlated with hypoxia signature in all 25 cancer tissues (r > 0.7) and cancer single cells (r > 0.8). In addition, HSPA8 and P4HA1 were screened out as the potential modulating factors to glycolysis as their expression were highly correlated with glycolysis score and glycolysis genes, which enables future efforts for therapeutic options to block the glycolysis and control tumor progression. Our study provides a comprehensive molecular-level understanding of glycolysis with a large sample data and demonstrates the hypoxia pressure, growth signals, oncogene mutation and other potential signals could activate glycolysis, thereby to regulate cell cycle, energy material synthesis, cell proliferation and cancer progression.

scholarly journals UBE2O targets Mxi1 for ubiquitination and degradation to promote lung cancer progression and radioresistance

2020 ◽  
Author(s):  
Yumei Huang ◽  
Xijie Yang ◽  
Yanwei Lu ◽  
Ye Zhao ◽  
Rui Meng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Progression ◽  
Erythroid Differentiation ◽  
Tumor Proliferation ◽  
Ubiquitin Protein Ligase ◽  
Protein Levels ◽  
Pharmacological Blockade ◽  
Cancer Tissues

Abstract UBE2O, an E2/E3 hybrid ubiquitin-protein ligase, has been implicated in the regulation of adipogenesis, erythroid differentiation, and tumor proliferation. However, its role in cancer radioresistance remains completely unknown. Here, we uncover that UBE2O interacts and targets Mxi1 for ubiquitination and degradation at the K46 residue. Furthermore, we show that genetical or pharmacological blockade of UBE2O impairs tumor progression and radioresistance in lung cancer in vitro and in vivo, and these effects can be restored by Mxi1 inhibition. Moreover, we demonstrate that UBE2O is overexpressed and negatively correlated with Mxi1 protein levels in lung cancer tissues. Collectively, our work reveals that UBE2O facilitates tumorigenesis and radioresistance by promoting Mxi1 ubiquitination and degradation, suggesting that UBE2O is an attractive radiosensitization target for the treatment of lung cancer.

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