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  • Open Access

    ARTICLE

    High expression of PD-L1 mainly occurs in non-small cell lung cancer patients with squamous cell carcinoma or poor differentiation

    LU LIU1,2, BIN XIE1,2, WEI ZHU1,2, QIUYAN HE1,2, JIANHUA ZHOU1,2, SHUANG LIU3, YONGGUANG TAO4, DESHENG XIAO1,2,*

    Oncology Research, Vol.31, No.3, pp. 275-286, 2023, DOI:10.32604/or.2023.028227

    Abstract Background: Lung cancer is one of the most lethal cancers worldwide, but studies have shown that the higher the expression of programmed cell death protein 1 ligand 1 (PD-L1) in non-small cell lung cancer (NSCLC), the more likely it will benefit from anti-PD-L1 immunotherapy. The purpose of our study was to collect and analyze abundant clinical samples in order to provide evidence for clinicians and patients who might consider anti-PD-L1 immunotherapy while jointly formulating treatment plans. Methods: On the one hand, we obtained cases from The Cancer Genome Atlas (TCGA) database, including 498 lung squamous cell cancer (LUSC) patients and… More >

  • Open Access

    REVIEW

    Advances in Targeted Therapy Against Driver Mutations and Epigenetic Alterations in Non-Small Cell Lung Cancer

    Jiajian Shi1, Yuchen Chen1,*, Chentai Peng1, Linwu Kuang2, Zitong Zhang1, Yangkai Li2,*, Kun Huang1

    Oncologie, Vol.24, No.4, pp. 613-648, 2022, DOI:10.32604/oncologie.2022.027545

    Abstract The incidence and mortality of lung cancer rank top three of all cancers worldwide. Accounting for 85% of the total number of lung cancer, non-small cell lung cancer (NSCLC) is an important factor endangering human health. Recently, targeted therapies against driver mutations and epigenetic alterations have made encouraging advances that benefit NSCLC patients. Druggable driver mutations, which mainly occur in EGFR, KRAS, MET, HER2, ALK, ROS1, RET and BRAF, have been identified in more than a quarter of NSCLC patients. A series of highly selective mutant targeting inhibitors, such as EGFR tyrosine kinase inhibitors and KRAS inhibitors, have been well… More >

  • Open Access

    ARTICLE

    GABPB1-AS1 acts as a tumor suppressor and inhibits non-small cell lung cancer progression by targeting miRNA-566/F-box protein 47

    HUALIANG LV1,#,*, CHANGCHUN LAI2,#, WENQU ZHAO3, YIBO SONG1

    Oncology Research, Vol.29, No.6, pp. 401-409, 2021, DOI:10.32604/or.2022.025262

    Abstract It has been certified that GABPB1-AS1 is aberrantly expressed and plays as a vital role in some kinds of cancers. However, its expression pattern and functions in non-small cell lung cancer (NSCLC) are still largely unknown. This study aims to assess GABPB1-AS1 expression and biological roles in NSCLC. The expression of GABPB1-AS1 was detected in NSCLC specimens and adjacent normal specimens. CCK8 and Transwell assays were performed to evaluate the effects of GABPB1-AS1 on NSCLC cell proliferation, migration and invasion. Bioinformatics tools and luciferase reporter assays were applied to predict and verify GABPB1-AS1’s direct targets. The results revealed that GABPB1-AS1… More >

  • Open Access

    ARTICLE

    MiR-21/Sonic Hedgehog (SHH)/PI3K/AKT Pathway is Associated with NSCLC of Primary EGFR-TKI Resistance

    Li Xu, Kang Li, Jia Li, Liyu Liu, Fang Xu, Yan Xu, Yi Kong, Xingxiang Pu, Qianzhi Wang, Jingyi Wang, Bolin Chen*, Lin Wu*

    Oncologie, Vol.24, No.3, pp. 579-590, 2022, DOI:10.32604/oncologie.2022.022121

    Abstract Background: Non-small cell lung cancer (NSCLC), caused by abnormal gene drive, may have primary drug resistance after treatment with tyrosine kinase inhibitors (EGFR-TKIs). Therefore, we explore whether the primary drug-resistant NSCLC treated with EGFR-TKI is related to the miR-21/Sonic Hedgehog (SHH)/PI3K/AKT pathway. Methods: The patients from our hospital who meet the AJCC TNM staging (7th edition) stage IIIB and stage IV NSCLC were selected in this case study. Thereafter, the treatment response of EGFR-TKIs was evaluated according to the solid tumor efficacy evaluation standard (version 1.1). The patients were divided into the EGFR-TKIs primary drug resistance group (EGFR-TKIs-Primary-R) and the… More >

  • Open Access

    ARTICLE

    Long noncoding RNA TFAP2A-AS1 exerts promotive effects in non-small cell lung cancer progression via controlling the microRNA-548a-3p/CDK4 axis as a competitive endogenous RNA

    YANG ZHANG, LIXIA MA, TINGTING ZHANG, PEIDONG LI, JIABIN XU, ZHUO WANG*

    Oncology Research, Vol.29, No.2, pp. 129-139, 2021, DOI:10.32604/or.2022.03563

    Abstract In this study, we mainly focus on probing expression profile and detailed functions of long non-coding RNA TFAP2A antisense RNA 1 (TFAP2A-AS1) in non-small cell lung cancer (NSCLC). Moreover, the mechanisms played by TFAP2A-AS1 were unraveled comprehensively. Herein, a notable overexpressed TFAP2A-AS1 in NSCLC was observed by TCGA and our own cohort. An increased TFAP2A-AS1 level displayed a negative correlation with the overall survival of patients with NSCLC. Loss-of-function approaches illustrated that the absence of TFAP2A-AS1 weakened NSCLC cell proliferation, colony formation, migration and invasion in vitro. Also, interference of TFAP2A-AS1 caused in vivo tumor growth suppression. Mechanistically, TFAP2A-AS1 could… More >

  • Open Access

    ARTICLE

    Knockdown of Long Noncoding RNA ENST457720 Inhibits Proliferation of Non-Small Cell Lung Cancer Cells In Vitro and In Vivo

    Jia Yu, Qiyu Fang, Shuyan Meng

    Oncology Research, Vol.27, No.1, pp. 47-53, 2019, DOI:10.3727/096504018X15193843443255

    Abstract Non-small cell lung cancer (NSCLC) represents the leading cause of cancer-related mortality worldwide. More and more reports have identified important roles for long noncoding RNAs (lncRNAs) in cancer development. ENST457720 expression was upregulated in lung adenocarcinoma in a microarray-based lncRNA screen. We determined the expression levels of ENST457720 in NSCLC tissues with quantitative real-time PCR and then studied their clinical significance. We explored the biological significance of ENST457720 with gain- and lossof-function analyses in vitro and in vivo. In this study, ENST457720 was expressed at higher levels in NSCLC tissues than in paired normal tissues. Higher ENST457720 expression was associated… More >

  • Open Access

    ARTICLE

    MicroRNA 615-3p Inhibits the Tumor Growth and Metastasis of NSCLC via Inhibiting IGF2

    Jiangtao Liu*, Yanli Jia*, Lijuan Jia*, Tingting Li, Lei Yang, Gongwen Zhang

    Oncology Research, Vol.27, No.2, pp. 269-279, 2019, DOI:10.3727/096504018X15215019227688

    Abstract MicroRNAs are essential regulators of cancer-associated genes at the posttranscriptional level, and their expression is altered in cancer tissues. Herein we sought to identify the regulation of miR-615-3p in NSCLC progression and its mechanism. miR-615-3p expression was significantly downregulated in NSCLC tissue compared to control normal tissue. Exogenous overexpression of miR-615-3p inhibited the growth and metastasis of NSCLC cells. In addition, the in vivo mouse xenograft model showed that overexpression of miR- 615-3p inhibited NSCLC growth and lung metastasis, whereas decreased expression of miR-615-3p caused an opposite outcome. Furthermore, we revealed that insulin-like growth factor 2 (IGF2) expression was negatively… More >

  • Open Access

    ARTICLE

    miR-223-5p Suppresses Tumor Growth and Metastasis in Non-Small Cell Lung Cancer by Targeting E2F8

    Liyan Dou*1, Kaiyu Han†1, Mochao Xiao*, Fuzhen Lv

    Oncology Research, Vol.27, No.2, pp. 261-268, 2019, DOI:10.3727/096504018X15219188894056

    Abstract miR-223-5p has been demonstrated to regulate the development and progression of various cancers, such as hepatocellular carcinoma, breast cancer, and gastric carcinoma. However, the role of miR-223-5p in nonsmall cell lung cancer (NSCLC) requires further investigation. In this study, we found that the expression of miR-223-5p was significantly downregulated in NSCLC tissues and cell lines. Moreover, the expression level of miR-223-5p is negatively correlated with the malignance of NSCLC. We found that overexpression of miR-223-5p remarkably suppressed the proliferation of NSCLC cells in vitro and in vivo. miR-223-5p overexpression also led to reduced migration and invasion in NSCLC cells. Mechanistically,… More >

  • Open Access

    ARTICLE

    miR-449a Suppresses Tumor Growth, Migration, and Invasion in Non-Small Cell Lung Cancer by Targeting a HMGB1-Mediated NF-kB Signaling Pathway

    Dandan Wu*1, Jun Liu†1, Jianliang Chen*, Haiyan He*, Hang Ma*, Xuedong Lv*

    Oncology Research, Vol.27, No.2, pp. 227-235, 2019, DOI:10.3727/096504018X15213089759999

    Abstract MicroRNAs (miRNAs) have been reported to be involved in many human cancers and tumor progression. The dysregulation of miR-449a is found in many types of malignancies and is associated with tumor growth, migration, and invasion. However, its expression and function in non-small cell lung cancer (NSCLC) still remains unclear. In our study, miR-449a was found to be downregulated in both NSCLC tissues and cell lines, and low miR-449a expression was obviously associated with tumor differentiation, TMN stage, and poor overall survival (OS). Moreover, we demonstrated that miR-449a could inhibit tumor proliferation, migration, and invasion in NSCLC. We also confirmed that… More >

  • Open Access

    ARTICLE

    miR-185 Inhibits the Proliferation and Invasion of Non-Small Cell Lung Cancer by Targeting KLF7

    Lili Zhao*, Yao Zhang*, Jiaoxia Liu*, Wei Yin, Dan Jin, Dandan Wang*, Wei Zhang*

    Oncology Research, Vol.27, No.9, pp. 1015-1023, 2019, DOI:10.3727/096504018X15247341491655

    Abstract MicroRNAs (miRNAs) are short endogenous noncoding RNAs that frequently play vital roles in many cancer types. Herein we demonstrated that miR-185 was remarkably downregulated in NSCLC tissues compared with adjacent normal tissues. A lower level of miR-185 was associated with lymph node metastasis. Functional assays showed that upregulation of miR-185 inhibited the proliferation, colony formation, and invasion capacities of NSCLC cells in vitro. Furthermore, we found that miR-185 suppressed the epithelial–mesenchymal transition (EMT) process. Bioinformatics analysis and luciferase reporter gene assays revealed that Kruppellike factor 7 (KLF7) was the target of miR-185. Overexpression of miR-185 reduced the expression of KLF7… More >

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