scholarly journals Inhibiting of Proliferation, Migration, and Invasion in Lung Cancer Induced by Silencing Interferon-Induced Transmembrane Protein 1 (IFITM1)

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Jun Yan ◽  
Ying Jiang ◽  
Jianfeng Lu ◽  
Jianhui Wu ◽  
Mingfang Zhang
Keyword(s):  
Lung Cancer ◽  
Transmembrane Protein ◽  
Tumor Promoter ◽  
Migration And Invasion ◽  
Cellular Functions ◽  
Protein Levels ◽  
Cancer Tissues

Interferon-induced transmembrane protein 1 (IFITM1), a 17-kDa membrane protein, is generally known as a modulator in many cellular functions. Recent studies showed overexpression of IFITM1 in cancers and relationship between IFITM1 overexpression and tumor progression. However, the role of IFITM1 in lung cancer remains unclear. Here, we presented the overexpression of IFITM1 in lung cancer tissues and cell lines A549 and H460 using quantitative Real-Time RT-PCR.In vitroassay indicated IFITM1 silencing inhibited lung cancer cell proliferation, migration, and invasion. Further,in vivoassay showed that IFITM1 silencing markedly suppressed cell growth and metastasis of lung cancer in tumor-bearing BALB/c nude mice. Mechanistically, we found that IFITM1 silencing significantly alleviated the protein levels ofβ-catenin, cyclin D1, and c-Mycin lung cancer cells and tumor samples. Taken together, our study revealed the role of IFITM1 as a tumor promoter during lung cancer development and the possible molecular mechanism.

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 PATH-14. FHL1 INTERACTS WITH SP1 TO REGULATE EGFR EXPRESSION IN GLIOBLASTOMA

2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii167-ii167
Author(s):  
Lili Sun ◽  
Ming Li
Keyword(s):  
Brain Cancer ◽  
Tumor Suppressor Protein ◽  
Migration And Invasion ◽  
Lim Domain ◽  
Protein Levels ◽  
Stat3 Signaling ◽  
Egfr Expression

Abstract The four and a half LIM domain 1 (FHL1) has been considered as a tumor suppressor protein in multiple cancers. Here, we show that FHL1 plays a tumor-promoting role in glioblastoma, the most common and incurable brain cancer. Overexpression of FHL1 promotes the growth, migration, and invasion of GBM cells in vivo and in vitro. In contrast, FHL1 silencing exhibits the opposite effects. Mechanically, FHL1 upregulates EGFR expression and activates the downstream AKT / ERK1 / 2 / STAT3 signaling pathways. We further demonstrated that SP1 can also be induced by FHL1 expression, and FHL1 interacts with SP1 to upregulate EGFR expression at both mRNA and protein levels, leading to glioblastoma malignancy. Clinically, FHL1 is highly expressed in glioblastoma and shows positive correlation with EGFR and SP1 in GBM specimens. Our results suggest the key role of FHL1 in the expression of EGFR and highlight the translation potential of inhibiting FHL1 as a treatment for glioblastoma.

Hsa_circ_0003288 facilitates tumor progression by targeting miR-145 in non–small cell lung cancer cells

2021 ◽  
pp. 1-9
Author(s):  
Li-Na Pan ◽  
Yun-Fang Ma ◽  
Jia-An Hu ◽  
Zhi-Hong Xu
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Migration And Invasion ◽  
Small Cell Lung

Circular RNA (circRNA) has been shown to participate in various tumors, including lung cancer. In the present study, we explored the expression and functional relevance of hsa_circ_0003288 in human non-small cell lung cancer (NSCLC). We verified that hsa_circ_0003288 expression was upregulated in lung cancer tissues and cell lines. Overexpression of hsa_circ_0003288 dramatically promoted lung cancer cell proliferation, colony formation, inhibited apoptosis, and increased cell migration and invasion in vitro. Xenograft experiments showed that hsa_circ_0003288 overexpression accelerated tumor growth in vivo. Mechanistically, hsa_circ_0003288 negatively regulated miR-145 to exert the oncogenic role in lung cancer. Overexpression of miR-145 decreased cell proliferation, induced apoptosis, and suppressed migration and invasion in lung cancer. Additionally, miR-145 co-transfection abolished the oncogenic role of hsa_circ_0003288. Collectively, these findings identified a novel regulatory role of hsa_circ_0003288/miR-145 axis in the progression of NSCLC.

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.

scholarly journals LncRNA SNHG19 Promotes the Development of Non-Small Cell Lung Cancer via Mediating miR-137/E2F7 Axis

2021 ◽  
Vol 11 ◽  
Author(s):  
Guang-Yin Zhao ◽  
Zhao-Feng Ning ◽  
Rui Wang
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Small Cell Lung ◽  
Cancer Tissues

ObjectiveNon-small cell lung cancer (NSCLC) is a common malignant tumor, which has high incidence and low the 5-year survival rate. Long non-coding RNAs (lncRNAs) play critical roles in carcinoma occurrence and metastasis. Herein, our aim was to investigate the effects of lncRNA SNHG19 in NSCLC progression.Materials and MethodsLong non-coding RNA Small Nucleolar RNA Host Gene 19 (lncRNA SNHG19) expression level was measured by bioinformatics and qRT-PCR. Edu, Transwell, and scratch assays were performed to explore the role of si-SNHG19 or SNHG19 on NSCLC progression. Luciferase assay was used to verify the relationship between SNHG19/E2F7 and miR-137. The experiment of Xenograft was used for exploring the function of SNHG19 in vivo.ResultsSNHG19 was upregulated in cancer tissues, patients plasma and cell lines of NSCLC. Knockdown of SNHG19 inhibited cell proliferation, migration, and invasion. Luciferase assay confirmed that SNHG19 regulated E2F7 expression via interacting with miR-137. Overexpression of SNHG19 accelerated NSCLC tumor progression via miR-137/E2F7 axis both in vitro and in vivo.ConclusionsOur results clarified the SNHG19 function for the first time, and SNHG19 promoted the progression of NSCLC, which was mediated by the miR-137/E2F7 axis. This study might provide new understanding and targets for NSCLC diagnosis and treatment.

scholarly journals MicroRNA-215-3p Suppresses the Growth, Migration, and Invasion of Colorectal Cancer by Targeting FOXM1

2019 ◽  
Vol 18 ◽  
pp. 153303381987477 ◽  
Author(s):  
Xiaowei Tang ◽  
Xianfeng Shi ◽  
Nianfei Wang ◽  
Wanren Peng ◽  
Zhendong Cheng
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cell ◽  
Vital Role ◽  
Colorectal Cancer Cell ◽  
Migration And Invasion ◽  
Forkhead Box ◽  
Cancer Tissues

Previous investigations have indicated that microRNA-215-3p is dysregulated in many kinds of cancers and functions as oncogene or tumor suppressor. However, the potential role of microRNA-215-3p in the progression of colorectal cancer remains not well known. Herein, we demonstrated that microRNA-215-3p was downregulated in human colorectal cancer tissues and was reversely correlated to the lymph node metastasis of colorectal cancer. Overexpression of microRNA-215-3p inhibited the clonogenic abilities and metastasis-relevant traits of colorectal cancer cell in vitro. Consistently, upregulation of microRNA-215-3p inhibited the growth and metastasis of colorectal cancer cell in vivo. Forkhead box protein M1 was identified as a direct target of microRNA-215-3p and reexpression of forkhead box protein M1 reversed the suppressive impacts of microRNA-215-3p on the growth, mobility, and invasion abilities of colorectal cancer cell. Altogether, these results revealed the vital role of microRNA-215-3p in the tumorigenesis and metastasis of colorectal cancer.

scholarly journals LINC-PINT impedes DNA repair and enhances radiotherapeutic response by targeting DNA-PKcs in nasopharyngeal cancer

2021 ◽  
Vol 12 (5) ◽  
Author(s):  
You-hong Wang ◽  
Zhen Guo ◽  
Liang An ◽  
Yong Zhou ◽  
Heng Xu ◽  
...  
Keyword(s):  
Dna Damage ◽  
Nasopharyngeal Cancer ◽  
Noncoding Rnas ◽  
Dependent Protein Kinase ◽  
Damage Repair ◽  
Dependent Protein ◽  
Cancer Tissues

AbstractRadioresistance continues to be the leading cause of recurrence and metastasis in nasopharyngeal cancer. Long noncoding RNAs are emerging as regulators of DNA damage and radioresistance. LINC-PINT was originally identified as a tumor suppressor in various cancers. In this study, LINC-PINT was significantly downregulated in nasopharyngeal cancer tissues than in rhinitis tissues, and low LINC-PINT expressions showed poorer prognosis in patients who received radiotherapy. We further identified a functional role of LINC-PINT in inhibiting the malignant phenotypes and sensitizing cancer cells to irradiation in vitro and in vivo. Mechanistically, LINC-PINT was responsive to DNA damage, inhibiting DNA damage repair through ATM/ATR-Chk1/Chk2 signaling pathways. Moreover, LINC-PINT increased radiosensitivity by interacting with DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and negatively regulated the expression and recruitment of DNA-PKcs. Therefore, these findings collectively support the possibility that LINC-PINT serves as an attractive target to overcome radioresistance in NPC.

scholarly journals Circular RNA FLNA acts as a sponge of miR-486-3p in promoting lung cancer progression via regulating XRCC1 and CYP1A1

2021 ◽  
Author(s):  
Jiongwei Pan ◽  
Gang Huang ◽  
Zhangyong Yin ◽  
Xiaoping Cai ◽  
Enhui Gong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Lung Cancer Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Related Factors

AbstractSignificantly high-expressed circFLNA has been found in various cancer cell lines, but not in lung cancer. Therefore, this study aimed to explore the role of circFLNA in the progression of lung cancer. The target gene of circFLNA was determined by bioinformatics and luciferase reporter assay. Viability, proliferation, migration, and invasion of the transfected cells were detected by CCK-8, colony formation, wound-healing, and transwell assays, respectively. A mouse subcutaneous xenotransplanted tumor model was established, and the expressions of circFLNA, miR-486-3p, XRCC1, CYP1A1, and related genes in the cancer cells and tissues were detected by RT-qPCR, Western blot, or immunohistochemistry. The current study found that miR-486-3p was low-expressed in lung cancer. MiR-486-3p, which has been found to target XRCC1 and CYP1A1, was regulated by circFLNA. CircFLNA was located in the cytoplasm and had a high expression in lung cancer cells. Cancer cell viability, proliferation, migration, and invasion were promoted by overexpressed circFLNA, XRCC1, and CYP1A1 but inhibited by miR-486-3p mimic and circFLNA knockdown. The weight of the xenotransplanted tumor was increased by circFLNA overexpression yet reduced by miR-486-3p mimic. Furthermore, miR-486-3p mimic reversed the effect of circFLNA overexpression on promoting lung cancer cells and tumors and regulating the expressions of miR-486-3p, XRCC1, CYP1A1, and metastasis/apoptosis/proliferation-related factors. However, overexpressed XRCC1 and CYP1A1 reversed the inhibitory effect of miR-486-3p mimic on cancer cells and tumors. In conclusion, circFLNA acted as a sponge of miR-486-3p to promote the proliferation, migration, and invasion of lung cancer cells in vitro and in vivo by regulating XRCC1 and CYP1A1.

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.

Homeobox-A13 acts as a functional prognostic and diagnostic biomarker via regulating P53 and Wnt signaling pathways in lung cancer

2021 ◽  
pp. 1-16
Author(s):  
Yang Wang ◽  
Bo He ◽  
Yan Dong ◽  
Gong-Jin He ◽  
Xiao-Wei Qi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Signaling Pathways ◽  
Cox Regression ◽  
Prognostic Significance ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Clinical Feature ◽  
Diagnostic Biomarker

BACKGROUND: The prognosis of lung cancer patients is poor without useful prognostic and diagnostic biomarker. To search for novel prognostic and diagnostic markers, we previously found homeobox-A13 (HOXA13) as a promising candidate in lung cancer. OBJECTIVE: To determine the precisely clinical feature, prognostic and diagnostic value, possible role and mechanism of HOXA13. METHODS: Gene-expression was explored by real-time quantitative-PCR, western-blot and tissue-microarray. The associations were analyzed by Chi-square test, Kaplan-Meier and Cox-regression. The roles and mechanisms were evaluated by MTS, EdU, transwell, xenograft tumor and luciferase-reporter assays. RESULTS: HOXA13 expression is increased in tumors, and correlated with age of patients. HOXA13 expression is associated with unfavorable overall survival and relapse-free survival of patients in four cohorts. Interestingly, HOXA13 has different prognostic significance in adenocarcinoma (ADC) and squamous-cell carcinoma (SCC), and is a sex- and smoke-related prognostic factor only in ADC. Importantly, HOXA13 can serve as a diagnostic biomarker for lung cancer, especially for SCC. HOXA13 can promote cancer-cell proliferation, migration and invasion in vitro, and facilitate tumorigenicity and tumor metastasis in vivo. HOXA13 acts the oncogenic roles on tumor growth and metastasis by regulating P53 and Wnt/β-catenin signaling activities in lung cancer. CONCLUSIONS: HOXA13 is a new prognostic and diagnostic biomarker associated with P53 and Wnt/β-catenin signaling pathways.

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