The subjects carrying the TT genotype had a decreased risk of lung cancer in MMP9-1562C/T comparing with the CC genotype (<i>p</i> = 0.00, OR = 0.45, 95% CI = 0.29⁻0.68), and the MMP13-77 AA genotype was associated with a decreased risk of NSCLC by comparing with the GG genotype (<i>p</i> = 0.03, OR = 0.56, 95% CI = 0.33⁻0.94).
Naringenin inhibits the migration of bladder and lung cancer via modulation of MMP-2 and/or MMP-9 activities, Naringenin inhibits migration and trigger apoptosis in gastric cancer cells through downregulation of AKT pathway.
Comparison of the effects of sevoflurane and propofol anesthesia on pulmonary function, MMP-9 and postoperative cognition in patients receiving lung cancer resection.
Additionally, TRIM32 overexpression promoted lung cancer cell proliferation and motility and mediated the expression of Bax, Bcl-2, cleaved caspase-3, matrix metalloproteinase-2 (MMP-2) and MMP-9 were inhibited by JAK2/STAT3 signaling inhibitor (AG490).
The present study intended to investigate efficacy of radiotherapy in the treatment of intermediate and advanced stage lung cancer and the effects on serum vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9).
CONCLUSIONS The putative mechanism behind the metastasis-limiting effects of DHC may involve the suppression of Akt/GSK-3β and inhibition of MMP-2 and MMP-9 in lung cancer cells.
Among them, MMP9 and TWIST1 were identified as more valuable biological targets for the early diagnosis and targeted therapy of lung cancer through Kaplan-Meier analysis of TCGA lung adenocarcinoma datasets.
In summary, our results reveal the molecular mechanism of Aldolase A in promoting lung cancer metastasis via PHD-mediated stabilization of HIF-1α and the subsequent activation of MMP9.
MMP-9 gene could promote the generation of lung cancer through P13K/AKT signal pathway, which provides certain theoretical and experimental basis for subsequent diagnosis and treatment of lung cancer.
The present study indicated that FZKA may inhibit lung cancer metastasis via the STAT3/MMP9 pathway and EMT, suggesting that FZKA may serve as a novel promising therapeutic strategy for the treatment of patients with late stage lung cancer.
We first found that MRSA infection can enhance metastasis ability of A549 cell and increase matrix metalloproteinase (MMP2 and MMP9) expressions in MRSA-infected A549 cell.
Collectively, this study highlights the importance of the S100A4/NF-κB/MMP9 axis in lung cancer invasion and provides a rationale for targeting S100A4 to combat lung cancer.
Further experiments revealed that the NF-κB signal pathway inhibitor PDTC inhibited the upregulated expression of MMP9 induced by PHP14 overexpression in lung cancer cells.
Therefore, this meta-analysis suggests that the MMP1-1607 1G/2G, MMP2-1306 C/T, MMP2-735 C/T, MMP9-1562 C/T polymorphisms were risk factors for lung cancer among Asians, while MMP13 -77A/G polymorphism was not associated with lung cancer risk.
Moreover, the alteration of MMP-2, MMP-9, TGF-β and epidermal growth factor receptor (EGFR) expression, associated with the migration and metastasis potential of lung cancer cell lines, was identified by western blot analysis in transfected cells.
For example, matrix metalloproteinase 9 (MMP9) is overexpressed in tumors, is known to enhance the metastatic potency of malignant cells, and has been associated with poor prognosis of lung cancer.
In conclusion, we report that the shRNA-mediated knockdown of RhoGDI2 induces the invasion and migration of lung cancer due to cross-talk with the PI3K/Akt pathway and MMP-9.