New strategies to develop new medications for lung cancer and metastasis

Zhao, Yujie; Adjei, Alex A.

doi:10.1007/s10555-015-9553-5

Cited by 12 publications

(8 citation statements)

References 70 publications

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“…Distant metastasis is the major factor that contributes to the failure of NSCLC therapy. The factors governing NSCLC metastasis are complicated, and the underlying mechanism remains unclear [5,6]. Thus, identifying new molecules that regulate NSCLC metastasis and revealing its underlying mechanism is beneficial to promote NSCLC therapy.…”

Section: Introductionmentioning

confidence: 99%

MiR-206 may suppress non-small lung cancer metastasis by targeting CORO1C

Liao

Peng

2020

Cell Mol Biol Lett

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Object: Non-small lung cancer (NSCLC), with a poor 5-year survival rate (16%), is the major type of lung cancer. Metastasis has been identified as the main factor that leads to NSCLC therapy failure. MiR-206 is a metastasis suppressor in many cancers, including colorectal cancer, renal cell carcinoma and breast cancer. However, the role of miR-206 in NSCLC metastasis and the underlying mechanism are still obscure. Methods: Quantitative reverse-transcription PCR (q-RT-PCR) assay was used to detect miR-206 mRNA of NSCLC tissues and lung cancer lines. The MTT assay, scratch wound healing assay, transwell migration assay and transwell invasion assay were conducted to illuminate the effect of miR-206 on A549 cells' proliferation, migration and invasion. Gaussia luciferase reporter assay, q-RT-PCR and western blotting assay were used to explore the underlying mechanism. Also, the A549 xenograft model was conducted to evaluate the anti-tumor effect of miR-206 in vivo. Results: The results showed that miR-206 expression was decreased in NSCLC tissues and lung cancer cells. Further research demonstrated that miR-206 inhibited the proliferation, migration and invasion of A549 cells via negatively regulating Coronin-1C (CORO1C), and CORO1C deletion significantly rescues the miR-206 mediated inhibitory effect on A549 cells. Moreover, miR-206 exhibited a perfect anti-tumor effect in the A549 xenograft model. Conclusion: Our study reveals that miR-206 functions as a tumor metastasis suppressor and sheds new light on the clinical significance of miR-206 in NSCLC therapy.

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Section: Introductionmentioning

confidence: 99%

MiR-206 may suppress non-small lung cancer metastasis by targeting CORO1C

Liao

Peng

2020

Cell Mol Biol Lett

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“…Lung cancer is the leading cause of cancer death worldwide; according to the estimated data from GLOBOCAN in 2012, one of five cancer deaths is due to lung cancer (1.59 million deaths, 19.4% of the total cancer deaths) (1). Despite significant progress in the development of new therapies for lung cancer, metastasis and therapeutic resistance remain the major determinants of lung cancer progression and high mortality (2).…”

Section: Introductionmentioning

confidence: 99%

Glucose-Regulated Protein 78 Signaling Regulates Hypoxia-Induced Epithelial–Mesenchymal Transition in A549 Cells

et al. 2019

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Objective: Metastasis and therapeutic resistance are the major determinants of lung cancer progression and high mortality. Epithelial–mesenchymal transition (EMT) plays a key role in the metastasis and therapeutic resistance. Highly expressed glucose-regulated protein 78 (GRP78) is a poor prognostic factor in lung cancer and possibly correlated with EMT. This study aims to examine whether the up-regulation of GRP78 is involved in EMT in lung adenocarcinoma and explore the underlying downstream molecular pathways.Study Design: EMT was assessed by analysis of cell morphology and expression of EMT protein markers in A549 cells under normoxia, hypoxia and silencing GRP78 conditions. The expression levels of Smad2/3, Src, and MAPK (p38, ERK, and JNK) proteins were examined by Western blot analysis under hypoxia and treatments with phosphorylation inhibitors.Results: Under hypoxic conditions, the EMT morphology significantly changed and the GRP78 expression was significantly up-regulated in A549 cells compared with those in normoxia control. The expression and phosphorylation levels of smad2/3, Src, p38, ERK, and JNK were also upregulated. When GRP78 was silenced, EMT was inhibited, and the levels of phospho-smad2/3, phospho-Src, phospho-p38, phospho-ERK, and phospho-JNK were suppressed. When the activation of Smad2/3, Src, p38, ERK, and JNK was inhibited, EMT was also inhibited. The inhibition effect on EMT by these phosphorylation inhibitors was found to be weaker than that of GRP78 knockdown.Conclusions: Hypoxia-induced EMT in A549 cells is regulated by GRP78 signaling pathways. GRP78 promotes EMT by activating Smad2/3 and Src/MAPK pathways. Hence, GRP78 might be a potential target for treatment of lung adenocarcinoma.

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“…Treatment of lung cancer still represents a major challenge since the presence of multiple modified pathways and the occurrence of therapy-induced mutations greatly limits efficacy (7). Development of second-generation kinase inhibitors, multitargeted combination therapy, and novel immune system-stimulating drugs may represent a novel strategy to reduce treatment failure (8).…”

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confidence: 99%

Metabolic Evaluation of Non–Small Cell Lung Cancer Patient–Derived Xenograft Models Using ¹⁸F-FDG PET: A Potential Tool for Early Therapy Response

et al. 2016

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Lung cancer heterogeneity makes response to therapy extremely hard to predict. Patient-derived xenografts (PDXs) are a reliable preclinical model that closely recapitulates the main characteristics of the parental tumors and may represent a useful asset for testing new therapies. Here, using PET imaging, we investigated whether lung cancer PDXs reproduce the metabolic characteristics of the corresponding parental tumors. Methods: We performed longitudinal 18 F-FDG PET studies on 9 different PDX groups obtained by implanting primary-cancer fragments harvested from patients into mice. The SUV max of each PDX was calculated and compared with the SUV max of the corresponding parental tumor. Results: Tumor growth rate and uptake varied among the different PDXs and confirmed the preservation of individual characteristics. The intragroup reproducibility of PET measurements was good. Furthermore, PDXs from tumors with a higher metabolic rate displayed a rank order of uptake similar to that of the parental tumors. Conclusion: PDXs reproduced the glucose metabolism of the parental tumors and therefore represent a promising preclinical model for the early assessment of therapy efficacy.

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New strategies to develop new medications for lung cancer and metastasis

Cited by 12 publications

References 70 publications

MiR-206 may suppress non-small lung cancer metastasis by targeting CORO1C

MiR-206 may suppress non-small lung cancer metastasis by targeting CORO1C

Glucose-Regulated Protein 78 Signaling Regulates Hypoxia-Induced Epithelial–Mesenchymal Transition in A549 Cells

Metabolic Evaluation of Non–Small Cell Lung Cancer Patient–Derived Xenograft Models Using ¹⁸F-FDG PET: A Potential Tool for Early Therapy Response

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New strategies to develop new medications for lung cancer and metastasis

Cited by 12 publications

References 70 publications

MiR-206 may suppress non-small lung cancer metastasis by targeting CORO1C

MiR-206 may suppress non-small lung cancer metastasis by targeting CORO1C

Glucose-Regulated Protein 78 Signaling Regulates Hypoxia-Induced Epithelial–Mesenchymal Transition in A549 Cells

Metabolic Evaluation of Non–Small Cell Lung Cancer Patient–Derived Xenograft Models Using 18F-FDG PET: A Potential Tool for Early Therapy Response

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Metabolic Evaluation of Non–Small Cell Lung Cancer Patient–Derived Xenograft Models Using ¹⁸F-FDG PET: A Potential Tool for Early Therapy Response