A systematic review of targeted agents for non-small cell lung cancer

Vestergaard, Hannah Holm; Christensen, Marcus R.; Lassen, Ulrik

doi:10.1080/0284186x.2017.1404634

Cited by 53 publications

(61 citation statements)

References 87 publications

(108 reference statements)

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“…However, clinical studies targeting ErbB2 mutations have yielded disappointing results. Elevated ErbB2 expression was found in many NSCLC patients, but the role of ErbB2 overexpression in lung cancer remains unclear . There are various pathways that are regulated by ErbB2 that are involved in EMT, migration, and invasion of cancers.…”

Section: Discussionmentioning

confidence: 99%

“…Elevated ErbB2 expression was found in many NSCLC patients, but the role of ErbB2 overexpression in lung cancer remains unclear. 34 There are various pathways that are regulated by ErbB2 that are involved in EMT, migration, and invasion of cancers. Among them, Rac1 activation-induced migratory enhancement by ErbB2 was reported in breast cancer and ovarian tumor cells.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA‐331‐3p inhibits epithelial‐mesenchymal transition by targeting ErbB2 and VAV2 through the Rac1/PAK1/β‐catenin axis in non‐small‐cell lung cancer

Zhu

Liu

et al. 2019

Cancer Science

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MicroRNAs have been reported to play critical roles in the regulation of non‐small‐cell cancer (NSCLC) development, but the role of microRNA (miR)‐331‐3p in NSCLC is still unclear. In this study, the expression levels of miR‐331‐3p in NSCLC tumor tissues and adjacent normal tissues were examined by quantitative RT‐PCR, and the relationship between miR‐331‐3p expression and patient clinicopathological characteristics was analyzed. The effects of miR‐331‐3p on epithelial‐mesenchymal transition (EMT), migration, and metastasis of NSCLC cells were determined in vitro and vivo. Direct functional targets of miR‐331‐3p were identified by luciferase reporter assay, western blot assay, immunohistochemical staining, and rescue assay. The downstream pathway regulated by miR‐331‐3p was identified by immunofluorescence, immunoprecipitation, and Rac1 activity examination. Our results showed that miR‐331‐3p was significantly downregulated in NSCLC tumor tissues and was correlated with clinicopathological characteristics, and miR‐331‐3p could be an independent prognostic marker for NSCLC patients. Furthermore, miR‐331‐3p significantly suppressed EMT, migration and metastasis of NSCLC cells in vitro and in vivo. Both ErbB2 and VAV2 were direct functional targets of miR‐331‐3p. The activities of Rac1, PAK1, and β‐catenin were regulated by miR‐331‐3p through ErbB2 and VAV2 targeting. These results indicated that miR‐331‐3p suppresses EMT, migratory capacity, and metastatic ability by targeting ErbB2 and VAV2 through the Rac1/PAK1/β‐catenin axis in NSCLC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MicroRNA‐331‐3p inhibits epithelial‐mesenchymal transition by targeting ErbB2 and VAV2 through the Rac1/PAK1/β‐catenin axis in non‐small‐cell lung cancer

Zhu

Liu

et al. 2019

Cancer Science

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“…7 Therefore, it is imperative to develop new therapeutics for this cancer. However, effective treatment of NSCLC is still lacking, particularly for advanced stage cancers.…”

mentioning

confidence: 99%

Downregulation of miR‐33b promotes non‐small cell lung cancer cell growth through reprogramming glucose metabolism miR‐33b regulates non‐small cell lung cancer cell growth

Zhai

Zhao

Lin

et al. 2018

J of Cellular Biochemistry

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Glucose metabolism is a common target for cancer regulation and microRNAs (miRNAs) are important regulators of this process. Here we aim to investigate a tumor‐suppressing miRNA, miR‐33b, in regulating the glucose metabolism of non‐small cell lung cancer (NSCLC). In our study, quantitative real‐time polymerase chain reaction (qRT‐PCR) showed that miR‐33b was downregulated in NSCLC tissues and cell lines, which was correlated with increased cell proliferation and colony formation. Overexpression of miR‐33b through miR‐33b mimics transfection suppressed NSCLC proliferation, colony formation, and induced cell‐cycle arrest and apoptosis. Meanwhile, miR‐33b overexpression inhibited glucose metabolism in NSCLC cells. Luciferase reporter assay confirmed that miR‐33b directly binds to the 3′‐untranslated region of lactate dehydrogenase A (LDHA). qRT‐PCR and Western blot analysis showed that miR‐33b downregulated the expression of LDHA. Moreover, introducing LDHA mRNA into cells over‐expressing miR‐33b attenuated the inhibitory effect of miR‐33b on the growth and glucose metabolism in NSCLC cells. Taken together, these results confirm that miR‐33b is an anti‐oncogenic miRNA, which inhibits NSCLC cell growth by targeting LDHA through reprogramming glucose metabolism.

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“…There are phase I and II clinical trials with PI3K inhibitors in solid tumors and NSCLC, respectively, as well as in castration-resistant prostate carcinoma requiring assessment of PTEN status. [7][8][9] PTEN is not only an important predictive biomarker for PI3K inhibition, but it has recently been reported that PTEN-might be a mechanism of resistance to cancer immunotherapy, for example, in metastatic uterine leiomyosarcoma. 10 In mouse melanoma cells, PTENpromoted resistance to T cell-mediated immunotherapy such as anti-programmed death 1/programmed death ligand 1 (PD-L1), by decreasing T cell infiltration and expansion in tumors.…”

Section: Introductionmentioning

confidence: 99%

Computer-Based Intensity Measurement Assists Pathologists in Scoring Phosphatase and Tensin Homolog Immunohistochemistry — Clinical Associations in NSCLC Patients of the European Thoracic Oncology Platform Lungscape Cohort

Rulle

Tsourti

Casanova

et al. 2018

Journal of Thoracic Oncology

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A systematic review of targeted agents for non-small cell lung cancer

Abstract: This systematic review provides an overview of available literature in PubMed regarding NSCLC and TA. Included studies point toward that TA appears to be a promising therapeutic tool in treating NSCLC patients and use of TA is expected to result in improved treatment outcomes.

Cited by 53 publications

References 87 publications

MicroRNA‐331‐3p inhibits epithelial‐mesenchymal transition by targeting ErbB2 and VAV2 through the Rac1/PAK1/β‐catenin axis in non‐small‐cell lung cancer

MicroRNA‐331‐3p inhibits epithelial‐mesenchymal transition by targeting ErbB2 and VAV2 through the Rac1/PAK1/β‐catenin axis in non‐small‐cell lung cancer

Downregulation of miR‐33b promotes non‐small cell lung cancer cell growth through reprogramming glucose metabolism miR‐33b regulates non‐small cell lung cancer cell growth

Computer-Based Intensity Measurement Assists Pathologists in Scoring Phosphatase and Tensin Homolog Immunohistochemistry — Clinical Associations in NSCLC Patients of the European Thoracic Oncology Platform Lungscape Cohort

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