Matrix Metalloproteinase (MMP)-1 Induces Lung Alveolar Epithelial Cell Migration and Proliferation, Protects from Apoptosis, and Represses Mitochondrial Oxygen Consumption

Herrera, Iliana; Cisneros, José; Maldonado, M.; Ramı́rez, Remedios; Ortiz‐Quintero, Blanca; Ansó, Elena; Chandel, Navdeep S.; Selman, Moisés; Pardo, Annie

doi:10.1074/jbc.m113.459784

Cited by 97 publications

(67 citation statements)

References 33 publications

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“…HIF-1␣ activates transcription of genes encoding proteases that degrade the extracellular matrix including several MMPs, such as MMP-2, MMP-9, and MMP-14 (55). MMP-1 is also up-regulated when HIF-1␣ is induced by hypoxia in A549 epithelial cell line (56). HIF-1␣ promotes tumor metastasis into distant and more oxygenated tissues through the transcriptional activation of oncogenic growth factors such as TGF-␤3, EGF, and others.…”

Section: Discussionmentioning

confidence: 99%

Activation of Epidermal Growth Factor Receptor/p38/Hypoxia-inducible Factor-1α Is Pivotal for Angiogenesis and Tumorigenesis of Malignantly Transformed Cells Induced by Hexavalent Chromium

Kim¹,

Dai²,

Park³

et al. 2016

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

Activation of Epidermal Growth Factor Receptor/p38/Hypoxia-inducible Factor-1α Is Pivotal for Angiogenesis and Tumorigenesis of Malignantly Transformed Cells Induced by Hexavalent Chromium

Kim¹,

Dai²,

Park³

et al. 2016

Journal of Biological Chemistry

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“…In addition, MMP1 has been linked to the promotion of cell survival. The levels of MMP1 expression are associated with poor prognosis, suggesting that MMP1 may contribute to multiple processes during tumor growth and progression (Herrera et al 2013). MMPs mediate expansion of cells, which often leads to angiogenesis (Ma et al 2009).…”

Section: Discussionmentioning

confidence: 99%

The effects for PM2.5 exposure on non-small-cell lung cancer induced motility and proliferation

et al. 2016

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BackgroundIncreasing urbanization and associated air pollution, including elevated levels of particulate matter (PM), are strongly correlated with the development of various respiratory diseases. In particular, PM2.5 has been implicated in promoting lung cancer initiation, growth and progression. Cell migration and proliferation are crucial for the progression of cancer. However, the molecular signatures and biological networks representing the distinct and shared features of non-small cell lung cancer (NSCLC) after PM2.5 exposure are unknown.ResultsFunctional assays demonstrated higher proliferation, migration and invasion of cancer cells stimulated with PM2.5. To investigate the complicated mechanisms, we performed global transcriptome profiling of the A549 cell line. Particularly, transcriptome sequencing revealed invasive characteristics reminiscent of cancer cells. By comparing the transcriptomes, we identified distinct molecular signatures and cellular processes defining the invasive and proliferative properties of PM2.5-exposed cells, respectively. Interestingly, under the PM2.5-stimulated condition, the A549 and H1299 cells strengthened obviously properties in motility and proliferation. Based on the network model reconstructing the shared protein–protein interactions, we selected the two most up-regulated genes, interleukin-1β (IL1β) and matrix metalloprotease 1 (MMP1), as key regulators responsible for the effects of PM2.5 exposure. Notably, IL1β and MMP1 expression was elevated in independent assays, which was further enhanced by PM2.5.ConclusionTaken together, our systems approach to investigating PM2.5 exposure provides a basis to identify key regulators responsible for the pathological features of NSCLC.

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“…One of the limitations to our study is the use of alveolar type II cells from two different species. While we acknowledge that the species differences may play a role in the responses of these particular cells, both of these cell lines are derived from alveolar type II cells, are highly characterized, are the topics of numerous publications, and have been used previously to contrast cancer verses non-cancer lung epithelial cells (47, 48). A549 cells are derived from a lung carcinoma and possess the invasive characteristics of cancer cells while MLE12 cells are immortalized with the integration of the SV40 large T antigen and are not “normal cells” but are non-invasive and non-cancerous in nature.…”

Section: Discussionmentioning

confidence: 99%

Alterative Expression and Localization of Profilin 1/VASPpS157 and Cofilin 1/VASPpS239 Regulates Metastatic Growth and Is Modified by DHA Supplementation

Ali

Heyob

Jacob

et al. 2016

Molecular Cancer Therapeutics

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Profilin 1, cofilin 1, and vasodialator stimulated phosphoprotein (VASP) are actin binding proteins (ABP) which regulate actin remodelling and facilitate cancer cell metastases. MiR~17–92 is highly expressed in metastatic tumors and profilin1 and cofilin1 are predicted targets. Docosahexaenoic acid (DHA) inhibits cancer cell proliferation and adhesion. These studies tested the hypothesis that the metastatic phenotype is driven by changes in ABPs including alternative phosphorylation and/or changes in subcellular localization. Additionally, we tested the efficacy of DHA supplementation to attenuate or inhibit these changes. Human lung cancer tissue sections were analyzed for F-actin content and expression and cellular localization of profilin1, cofilin1 and VASP (S157 or S239 phosphorylation). The metastatic phenotype was investigated in A549 and MLE12 cells lines using 8 Br-cAMP as a metastasis inducer and DHA as a therapeutic agent. Migration was assessed by wound assay and expression measured by western blot and confocal analysis. MiR~17–92 expression was measured by qRT-PCR. Results indicated increased expression and altered cellular distribution of profilin1/VASPpS157 but no changes in cofilin1/VASPpS239 in the human malignant tissues compared to normal tissues. In A549 and MLE12 cells, the expression patterns of profilin1/VASPpS157 or cofilin1/VASPpS239 suggested an interaction in regulation of actin dynamics. Furthermore, DHA inhibited cancer cell migration and viability, ABP expression and cellular localization, and modulated expression of miR~17–92 in A549 cells with minimal effects in MLE12 cells. Further investigations are warranted to understand ABP interactions, changes in cellular localization, regulation by miR~17–92, and DHA as a novel therapeutic.

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Matrix Metalloproteinase (MMP)-1 Induces Lung Alveolar Epithelial Cell Migration and Proliferation, Protects from Apoptosis, and Represses Mitochondrial Oxygen Consumption

Cited by 97 publications

References 33 publications

Activation of Epidermal Growth Factor Receptor/p38/Hypoxia-inducible Factor-1α Is Pivotal for Angiogenesis and Tumorigenesis of Malignantly Transformed Cells Induced by Hexavalent Chromium

Activation of Epidermal Growth Factor Receptor/p38/Hypoxia-inducible Factor-1α Is Pivotal for Angiogenesis and Tumorigenesis of Malignantly Transformed Cells Induced by Hexavalent Chromium

The effects for PM2.5 exposure on non-small-cell lung cancer induced motility and proliferation

Alterative Expression and Localization of Profilin 1/VASPpS157 and Cofilin 1/VASPpS239 Regulates Metastatic Growth and Is Modified by DHA Supplementation

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