Correlation between MMP2 expression in lung cancer tissues and clinical parameters: a retrospective clinical analysis

Han, Liping; Sheng, Baowei; Zeng, Qi; Yao, Weirong; Jiang, Qiufang

doi:10.1186/s12890-020-01317-1

Cited by 49 publications

(45 citation statements)

References 26 publications

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“…MMP9 expression was reported to increase with tumor size and be significantly higher in metastatic NSCLC cases than in cases without metastasis [26]. Similarly, MMP2 expression in lung cancer tissues was shown to be higher than that found in normal tissues and suggested to be related to the development of lung cancer [29].…”

Section: Introductionmentioning

confidence: 99%

Differences in the Relative Abundance of ProBDNF and Mature BDNF in A549 and H1299 Human Lung Cancer Cell Media

Dorandish

Atali

Ray

et al. 2021

IJMS

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Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, has been linked to several human malignancies and shown to promote tumorigenesis. The purpose of this study was to explore the relative abundance of pro-brain-derived neurotrophic factor (proBDNF) and mature BDNF (mBDNF) in A549 (p53 wild-type) and H1299 (p53-null) lung cancer cell media. Higher levels of proBDNF were detected in the media of A549 cells than in H1299 cell media. Using inhibitors, we found that the levels of proBDNF and mBDNF in the media are likely regulated by PI3K, AKT, and NFκB. However, the largest change in these levels resulted from MMP2/9 inhibition. Blocking p53 function in A549 cells resulted in increased mBDNF and decreased proBDNF, suggesting a role for p53 in regulating these levels. The ratio of proBDNF/mBDNF was not affected by MMP2 knockdown but increased in the media of both cell lines upon knockdown of MMP9. Downregulation of either MMP2 or MMP9 by siRNA showed that MMP9 siRNA treatment of either A549 or H1299 cells resulted in decreased cell viability and increased apoptosis, an effect diminished upon the same treatment with proBDNF immunodepleted media, suggesting that MMP9 regulates the cytotoxic effects induced by proBDNF in lung cancer cells.

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Section: Introductionmentioning

confidence: 99%

Differences in the Relative Abundance of ProBDNF and Mature BDNF in A549 and H1299 Human Lung Cancer Cell Media

Dorandish

Atali

Ray

et al. 2021

IJMS

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“…In addition, we found that paclitaxel statistically significantly decreased the expression of EGF receptors in different lung cancer cells. Although paclitaxel can suppress the EGFR signaling pathways in different cancer cells most probably via matrix metalloproteinases [ 85 , 86 , 87 , 88 ], a direct suppression of EGF receptors, in our knowledge, was not previously reported. In our studies, paclitaxel treatment reduced only about 10–15% expression of the EGFR protein when compared to the vehicle-treated cells.…”

Section: Discussionmentioning

confidence: 97%

Multifunctional Lipid-Based Nanoparticles for Codelivery of Anticancer Drugs and siRNA for Treatment of Non-Small Cell Lung Cancer with Different Level of Resistance and EGFR Mutations

Majumder

Minko

2021

Pharmaceutics

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Resistance to chemotherapy, enhanced proliferation, invasion, angiogenesis, and metastasis (RPIAM) represent major obstacles that limit the efficacy of cancer treatment especially in advanced stages of cancer. Overcoming or suppressing RPIAM can dramatically improve the treatment outcome. Non-small cell lung cancer (NSCLC) is frequently diagnosed in an advanced stage and often possesses intrinsic resistance to chemotherapy accompanied by the fast development of acquired resistance during the treatment. Oncogenic receptor tyrosine kinases (TKs), specifically epidermal growth factor (EGF) TKs, play an important role in the activation of MAPK/PI3K/Akt/STAT pathways, finally leading to the development of RPIAM. However, the suppression of EGF-TK by different drugs is limited by various defensive mechanisms and mutations. In order to effectively prevent the development of RPIAM in NSCLC, we formulated and tested a multicomponent and multifunctional cancer targeted delivery system containing Nanostructured Lipid Carriers (NLCs) as vehicles, luteinizing hormone release hormone (LHRH) as a cancer targeting moiety, EFG-TK inhibitor gefitinib and/or paclitaxel as anticancer drug(s), siRNA targeted to EGF receptor (EGFR) mRNA as a suppressor of EGF receptors, and an imaging agent (rhodamine) for the visualization of cancer cells. Experimental data obtained show that this complex delivery system possesses significantly enhanced anticancer activity that cannot be achieved by individual components applied separately.

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“…Invasion-associated proteins MMP-2 (72 kDa gelatinase A) and MMP-9 (92 kDa gelatinase B) promote tumor invasion and metastasis through disruption of extracellular matrix (ECM) and induction of epithelial-mesenchymal transition (EMT) (27,28). High expressions of both MMP-2 and MMP-9 as unfavorable prognostic predictors were correlated with lymph node metastasis and poor prognosis in NSCLC patients (29,30). Our results demonstrated that the combination of regorafenib and cisplatin not only significantly reduced the number of migration and invasion cells, but also effectively abolished protein levels of both MMP-2 and MMP-9 compared to regorafenib or cisplatin monotherapy (Figure 3).…”

Section: Discussionmentioning

confidence: 99%

Induction of Apoptosis and Inhibition of EGFR/NF-κB Signaling Are Associated With Regorafenib-sensitized Non-small Cell Lung Cancer to Cisplatin

Chiou

Hsu

et al. 2021

In Vivo

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Background/Aim: The combination of regorafenib with cisplatin/pemetrexed has indicated controllable safety and encouraging antitumor activity in non-small cell lung cancer (NSCLC) patients. However, the anti-NSCLC effects and action mechanisms of regorafenib combined with cisplatin is ambiguous. The major goal of the study was to study the inhibitory effects and action mechanisms of regorafenib combined with cisplatin in NSCLC cells. Materials and Methods: Cell viability, flow cytometry, immunofluorescence staining, western blotting, migration, and invasion assays were employed to verify the anti-NSCLC effects and mechanisms of regorafenib in combination with cisplatin. Results: Cisplatin-induced epidermal growth factor receptor (EGFR)/nuclear factor ĸB (NF-ĸB) signaling was effectively inhibited by regorafenib treatment. Regorafenib, erlotinib (EGFR inhibitor) and QNZ (NF-ĸB inhibitor) may all enhance the cytotoxicity effect of cisplatin. The invasion ability was effectively decreased by combination treatment. Caspase-dependent and -independent apoptosis was activated by cisplatin combined with regorafenib. Conclusion: Apoptosis induction and EGFR/NF-ĸB inactivation correlate with regorafenib-enhanced anti-NSCLC efficacy of cisplatin.This study provides evidence of the therapeutic efficacy of regorafenib in combination with cisplatin on NSCLC.Cisplatin, a platinum-based anticancer drug, is standard treatment for advanced non-small cell lung cancer (NSCLC). DNA damage-induced apoptosis correlates with the anticancer mechanism of cisplatin (1, 2). Cell and animal models have revealed that enhancement of apoptosis induction and suppression of oncogenic signaling such as Wnt, AKT, epidermal growth factor receptor (EGFR), and nuclear factor-kappaB (NF-ĸB) by potential complementary approaches have been reported to sensitize NSCLC cells to cisplatin (3-6). For instance, sodium valproate, a histone deacetylase inhibitor, and microRNA miR-381 have been found to enhance anti-NSCLC efficacy of cisplatin through inducing apoptosis and inhibiting NF-ĸB signaling, respectively (7, 8).Several tyrosine kinase inhibitors (TKIs) targeting EGFR and anaplastic lymphoma kinase (ALK) have been shown to improve survival of NSCLC patients receiving platinum-based doublet chemotherapy (9, 10). Regorafenib, an oral multitarget TKI, is used for the treatment of solid tumors such as hepatocellular carcinoma (HCC), renal cell carcinoma, differentiated thyroid cancer, and metastatic colorectal cancer (11,12). Induction of apoptosis and down-regulation of AKT/NF-ĸB signaling were associated with regorafenibinhibited progression of NSCLC cells (13). In addition, the combination of regorafenib with cisplatin/pemetrexed has shown manageable tolerability and encouraging antitumor 2569 This article is freely accessible online.

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Correlation between MMP2 expression in lung cancer tissues and clinical parameters: a retrospective clinical analysis

Cited by 49 publications

References 26 publications

Differences in the Relative Abundance of ProBDNF and Mature BDNF in A549 and H1299 Human Lung Cancer Cell Media

Differences in the Relative Abundance of ProBDNF and Mature BDNF in A549 and H1299 Human Lung Cancer Cell Media

Multifunctional Lipid-Based Nanoparticles for Codelivery of Anticancer Drugs and siRNA for Treatment of Non-Small Cell Lung Cancer with Different Level of Resistance and EGFR Mutations

Induction of Apoptosis and Inhibition of EGFR/NF-κB Signaling Are Associated With Regorafenib-sensitized Non-small Cell Lung Cancer to Cisplatin

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