Concurrent Chemotherapy and Radiation Therapy for Inoperable Locally Advanced Non–Small-Cell Lung Cancer

Rosenzweig, Kenneth E.; Gomez, Jorge

doi:10.1200/jco.2016.69.9678

Cited by 38 publications

(34 citation statements)

References 30 publications

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“…Non‐small cell lung cancer (NSCLC) is the predominant type of lung cancer and accounts for approximately 85% of cases . Surgery, chemotherapy, radiotherapy, targeted therapy, and immunotherapy are used alone or in combination to treat NSCLC . The five‐year overall survival rate of NSCLC remains as low as 16% because most patients are already at a locally advanced or metastatic stage when diagnosed .…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA linc01433 promotes migration and invasion in non‐small cell lung cancer

et al. 2018

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BackgroundFor many years, lung cancer has been the most common and deadly cancer worldwide. Early diagnosis of non‐small cell lung cancer (NSCLC) in particular is very difficult because the symptoms are often ignored. The five‐year survival rate is very low despite great improvements to therapy. Thus, there is an urgent need to identify prognostic biomarkers and target molecules for the clinical diagnosis and individualized treatment of NSCLC.MethodsWe performed quantitative real‐time PCR to determine the expression levels of the long non‐coding RNA (lncRNA) linc01433 in NSCLC and normal matched lung tissue. Subsequently, we established cell lines with overexpression or knockdown of linc01433 to evaluate the effects on proliferation and metastasis in vitro. Epithelial‐to‐mesenchymal transition was examined using Western blot.ResultsLinc01433 was significantly overexpressed in NSCLC tissues compared to normal lung tissues. In addition, linc01433 levels were associated with smoking history. Linc01433 overexpression in lung cancer cells increased proliferation, migration, and invasion abilities, as well as epithelial‐to‐mesenchymal transition.ConclusionsLinc01433 is a cancer‐related lncRNA that may have an oncogene‐like effect in NSCLC.

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Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA linc01433 promotes migration and invasion in non‐small cell lung cancer

et al. 2018

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“…Nevertheless, despite the great efforts that have been exerted to develop radiation therapies for NSCLC patients, the 5-year overall survival rate still remains less than 15% [1, 5]. Local recurrence is a common clinical problem and is the primary contributor to the poor prognosis of a large number of patients [6]. One of the major reasons for local recurrence is the development of radiation resistance [7].…”

Section: Introductionmentioning

confidence: 99%

MiR-99a Enhances the Radiation Sensitivity of Non-Small Cell Lung Cancer by Targeting mTOR

Yin

Chen

et al. 2018

Cell Physiol Biochem

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Background/Aims: Radiation therapy is an important and effective modality for the treatment of non-small cell lung cancer (NSCLC). MicroRNAs (miRNAs) are crucial post-transcriptional regulators that are involved in numerous important biologic processes. However, their potential involvement in radiation sensitivity remains unknown. Materials: We performed integrated analysis of miRNA expression in NSCLC using The Cancer Genome Atlas datasets. miR-99a was found to be significantly upregulated in cancer tissue and regulated cell survival. Cell culture was used to assess the role of miR-99a in radiation sensitivity. We then used flow cytometry to examine the effects of miR-99a on the cell cycle and apoptosis in cells exposed to radiation. To identify gene targets of miR-99a, a bioinformatics approach was adopted, and the findings of this analysis were verified using luciferase reporter assays. Finally, an in vivo study was conducted to examine the effect of miR-99a on tumor volume in an NSCLC mouse model undergoing radiation therapy. Results: miR-99a was significantly upregulated in radiation-sensitive A549 cells compared with radiation-resistant A549 cells. miR-99a overexpression was shown to enhance radiosensitivity, while inhibition of miR-99a resulted in radioresistance of NSCLC cell lines in vitro and in vivo. In addition, by bioinformatics software analysis and luciferase assays, mammalian target of rapamycin (mTOR) was identified as a direct target of miR-99a. Furthermore, AZD2014, an inhibitor of mTOR, enhanced radiosensitivity and apoptosis in NSCLC cell lines, while mTOR overexpression resulted in radioresistance and cell survival from miR-99a-induced cell apoptosis. Moreover, miR-99a overexpression further increased the efficacy of radiation therapy in an NSCLC xenograft mouse model, and miR-99a and mTOR expression was significantly inversely correlated. Conclusions: Altogether, these data suggested miR-99a functions as a tumor suppressor that has a critical role in regulating radiosensitivity of NSCLC by targeting the mTOR signaling pathway.

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“…The standard treatment option of NSCLC is surgical resection combined with adjuvant radiotherapy/chemotherapy and molecule-targeted agents. However, many patients with NSCLC are diagnosed at a late stage and are not suitable for surgical treatment [2]. Currently, the molecular mechanisms of NSCLC progression are still incompletely understood and the treatment efficiency is far from what people expected.…”

Section: Introductionmentioning

confidence: 99%

TMEM100 negatively regulated by microRNA-106b facilitates cellular apoptosis by repressing survivin expression in NSCLC

Yan

Bai

et al. 2020

Preprint

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Background Non-small-cell lung cancer (NSCLC) is a common malignant tumor. Nevertheless, the 5-year survival rate of NSCLC patients remains poor. Thus, finding critical factors involved in regulating the progression of NSCLC is important for providing potential treatment targets. Methods CCK-8, colony formation, caspase-3 activity, luciferase reporter assay, and western blot assays were utilized in this study. Results We found that TMEM100 was significantly downregulated in NSCLC tissues compared with paired peritumoral tissues. Decreased TMEM100 expression was associated with poor clinical outcomes in NSCLC patients. Moreover, TMEM100 overexpression inhibited colony formation and facilitated apoptosis via repressing survivin expression in NSCLC cells, whereas TMEM100 knockdown had the opposite effect. In addition, miR-106b, a microRNA with controversial roles in different human cancers, was upregulated in NSCLC and directly downregulated TMEM100 expression. The roles of miR-106b in cell survival were mitigated by the restoration of TMEM100. Conclusions The above results indicate that TMEM100 induces cell apoptosis and inhibits cell survival by serving as a tumor suppressor and that miR-106b-degraded TMEM100 expression defines a potentially oncogenic pathway in NSCLC.

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Concurrent Chemotherapy and Radiation Therapy for Inoperable Locally Advanced Non–Small-Cell Lung Cancer

Cited by 38 publications

References 30 publications

Long non‐coding RNA linc01433 promotes migration and invasion in non‐small cell lung cancer

Long non‐coding RNA linc01433 promotes migration and invasion in non‐small cell lung cancer

MiR-99a Enhances the Radiation Sensitivity of Non-Small Cell Lung Cancer by Targeting mTOR

TMEM100 negatively regulated by microRNA-106b facilitates cellular apoptosis by repressing survivin expression in NSCLC

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