Prognostic value of number of negative lymph node in patients with stage II and IIIa non-small cell lung cancer

Wang, Shengguang; Zhang, Bin; Li, Chenguang; Cui, Chao; Yue, Dongsheng; Shi, Bowen; Zhang, Qiang; Zhang, Zhenfa; Zhang, Xi; Wang, Changli

doi:10.18632/oncotarget.18154

Cited by 12 publications

(13 citation statements)

References 37 publications

(33 reference statements)

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“…26 In addition, the number of lymph nodes examined was another important prognostic predictor for NSCLC. 27 Recent studies indicate that the ratio of positive lymph nodes and lymph nodes examined is a significant prognostic factor for NSCLC. 28 However, it was not appropriate for a nomogram and would potentially decrease the accuracy of the model.…”

Section: Discussionmentioning

confidence: 99%

A nomogram to predict the survival of stage IIIA-N2 non–small cell lung cancer after surgery

Mao

Xia

Dong

et al. 2018

The Journal of Thoracic and Cardiovascular Surgery

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Section: Discussionmentioning

confidence: 99%

A nomogram to predict the survival of stage IIIA-N2 non–small cell lung cancer after surgery

Mao

Xia

Dong

et al. 2018

The Journal of Thoracic and Cardiovascular Surgery

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“… 1 , 2 Due to a lack of valid diagnosis methods for early-onset lung cancer, most patients are unfortunately diagnosed at the later stages of the disease, when the prognosis is poor and where the 5-year survival rate is only about 15%. 3 There is now an imperative need for more research dedicated to the search for new tumor markers or therapeutic targets for lung cancer.…”

Section: Introductionmentioning

confidence: 99%

miR-1269 promotes cell survival and proliferation by targeting tp53 and caspase-9 in lung cancer

Bao¹,

Song²,

Xia³

et al. 2018

OTT

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Background and aimLung cancer is the leading cause of cancer death worldwide. In this study, we aim to elucidate the role of miR-1269 in the pathogenesis of lung cancer.Methods and resultsFrom the results of analyses using The Cancer Genome Atlas (TCGA) database, we noted the expression of miR-1269 was increased in lung cancer tissue. miR-1269 expression was detected in both the normal adjacent lung tissue and in the tumorous lung tissue of lung cancer patients, and miR-1269 was more highly expressed in the tumors. High expression of miR-1269 correlated with patients’ tumor stage and lymph node metastasis. A Cell Counting Kit-8 (CCK8) analysis and a cloning formation assay showed that overexpression of miR-1269 significantly promoted the growth of A549 cells, and that a lower expression of miR-1269 significantly increased cell apoptosis. We used the TargetScan 6.2 Database to predict the potential targets of miR-1269, and a luciferase activity assay was used to determine the direct interaction between miR-1269, tumor protein p53 (TP53), and caspase-9. Results from Western blots and real-time PCR showed that overexpression of miR-1269 significantly inhibited TP53 and caspase-9 expression. In addition, caspase-3 activity was found to decrease in a miR-1269 mimic group. The results showed that gene silencing of TP53 and caspase-9 significantly inhibited A549 cell growth and promoted cell apoptosis. The results also showed that the inhibition of miR-1269 and caspase-9 expression inhibited cell apoptosis. Immunohistochemistry (IHC) results demonstrated that TP53 and caspase-9 were expressed in low levels in tumor tissues, and that an inverse correlation exists between miR-1269 expression levels and TP53 or caspase-9 expression levels.ConclusionThese results demonstrate that miR-1269 promotes cell survival and proliferation by targeting TP53 and caspase-9 in lung cancer.

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“…In previous decades, with advances in surgical techniques and the development of chemical drug therapies, the outcomes of NSCLC patients have been improved (16). However, the 5-year survival rate of patients with NSCLC is only 15%, even following treatment (17). Therefore, determination of the molecular mechanism and development of novel therapeutic strategies are urgently required.…”

Section: Discussionmentioning

confidence: 99%

miR‑671‑3p is downregulated in non‑small cell lung cancer and inhibits cancer progression by directly targeting CCND2

Yao

Zhou

2019

Mol Med Report

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MicroRNAs (miRNAs) are implicated in the development and progression of non-small cell lung cancer (NSCLC). A previous study suggested that miR-671-3p suppresses the development of breast cancer. However, the role of miR-671-3p in NSCLC remains largely unknown. In the present study, it was identified that miR-671-3p was significantly upregulated in NSCLC tissues compared with adjacent normal tissues by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Similarly, decreased levels of miR-671-3p in NSCLC cell lines were observed compared with those in the non-tumorigenic human bronchial epithelial NL20 cell line. Cell Counting Kit-8 and Transwell invasion assays indicated that miR-671-3p overexpression suppressed the proliferation and invasion of A549 cells, and vice versa. Mechanistically, it was demonstrated that CCND2 was a direct target of miR-671-3p. RT-qPCR and western blot analysis indicated that miR-671-3p overexpression decreased the expression of CCND2 in A549 cells. Furthermore, rescue experiments demonstrated that the restoration of CCND2 may significantly reverse the suppressive roles of miR-671-3p overexpression on NSCLC cell proliferation and invasion. Taken together, the present study demonstrated that miR-671-3p exerted its tumor-suppressive roles via directly targeting CCND2 in NSCLC.

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Prognostic value of number of negative lymph node in patients with stage II and IIIa non-small cell lung cancer

Cited by 12 publications

References 37 publications

A nomogram to predict the survival of stage IIIA-N2 non–small cell lung cancer after surgery

A nomogram to predict the survival of stage IIIA-N2 non–small cell lung cancer after surgery

miR-1269 promotes cell survival and proliferation by targeting tp53 and caspase-9 in lung cancer

miR‑671‑3p is downregulated in non‑small cell lung cancer and inhibits cancer progression by directly targeting CCND2

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