From Proteomic Analysis to Potential Therapeutic Targets: Functional Profile of Two Lung Cancer Cell Lines, A549 and SW900, Widely Studied in Pre-Clinical Research

Korrodi‐Gregório, Luís; Soto‐Cerrato, Vanessa; Vitorino, Rui; Fardilha, Margarida; Pérez-Tomás, Ricardo

doi:10.1371/journal.pone.0165973

Cited by 45 publications

(26 citation statements)

References 96 publications

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“…Our data also confirm the presence of shared pathways with group A and GP7 enriched gene subsets, including many implicated in lung pathogenesis such as airway pathology, acute phase response signaling, and hepatic fibrosis. These findings are in line with current information on ARDS from the available curated literature genes [26,[45][46][47][48][49][50].…”

Section: Discussionsupporting

confidence: 90%

Characterizing a focused landscape of familial acute respiratory distress syndrome

Toby¹,

Thomas²,

Thorenoor³

et al. 2019

Preprint

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Background Acute respiratory distress syndrome (ARDS) affects approximately 190,600 patients per year in the United States, with mortality up to 45%. ARDS can occur as primary disease due to various factors (e.g. bacterial or viral pneumonia, gastric aspiration, lung contusion, toxic inhalation, and near drowning) or as secondary disease due to sepsis, pancreatitis, severe trauma, massive blood transfusion, and burn. We hypothesized that ARDS-affected individuals have patterns of variants in their physiological repertoire that can be tracked and utilized to complement clinical diagnosis and/or clinical monitoring. Methods The goals of this study were to: (1) characterize the landscape of variants within protein coding but we also studied UTR regions in ARDS using an Exome sequencing approach; (2), determine the variations in signaling pathways across ARDS; and (3) use computational approaches to explore the functional consequences of ARDS. Towards this we assessed an ARDS-affected individual in the context of unaffected individuals from the same family as well as unrelated ARDS cases, in order to elucidate underlying inheritance patterns of “private variants”. Private variants consist of variants shared by ARDS cases but not found in unaffected individuals. Results Whole exome sequencing yielded 3,516 variants represented by 2,354 genes. Of these, 128 variants were shared across all ARDS cases. Of these, there were 24 unique variants represented by 9 ARDS genes shared by the primary ARDS-case and unrelated individuals with ARDS. The overall genes identified and subsequent analysis, demonstrate that there are important biological pathways that distinguish ARDS cases from or from non-ARDS. These pathways include: cell-to-cell signaling interaction, cell growth and proliferation and cell morphology. The data also show a coordinated effort amongst biological processes such as liver hyperproliferation and cell death that underlie the pathogenesis of ARDS. Conclusions These in-silico discoveries demonstrate a role for private variants shared by ARDS cases to be leveraged as biomarkers for clinical diagnosis and/or monitoring of ARDS.

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Section: Discussionsupporting

confidence: 90%

Characterizing a focused landscape of familial acute respiratory distress syndrome

Toby¹,

Thomas²,

Thorenoor³

et al. 2019

Preprint

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“…Lung cancer is a malignant lung tumor characterized by uncontrolled lung cell proliferation (1). It is the most commonly diagnosed cancer and the leading cause of cancer-associated mortality (2).…”

Section: Introductionmentioning

confidence: 99%

Cryptotanshinone inhibits lung cancer invasion via microRNA‑133a/matrix metalloproteinase 14 regulation

Wang¹,

Zhang

et al. 2019

Oncol Lett

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Cryptotanshinone inhibits the proliferative and colony formation abilities of human non-small cell lung cancer cells (NSCLCs). The present study reported that signal transducer and activator of transcription 3 is not the only target of cryptotanshinone during the inhibition of human NSCLCs. It was identified that cryptotanshinone upregulates the expression levels of microRNA (miR)-30d-5p, miR-126-3p, miR-133a, miR-338-3p and miR-451a, and downregulates miR-21-5p, miR-96-5p, miR-182-5p and miR-205-5p. Among these, miR-133a was the most significantly upregulated. miR-133a targets and downregulates the expression of matrix metalloproteinase (MMP)14; however, MMP15, MMP16 and MMP24 were determined to be unaffected. This process was identified to be independent of tissue inhibitor of metalloproteinases 2. Cryptotanshinone also suppresses the invasion of human NSCLCs, which may be due to the inhibited expression of MMP14. In conclusion, cryptotanshinone may serve as a potential therapeutic agent in the treatment of lung cancer.

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“…ILF3 is overexpressed in lung carcinoma cells [23]. Stabilization of ILF3 protein by means of lncRNA-LET downregulation contributes to the hypoxia-induced lung cancer cell invasion [24].…”

Section: Resultsmentioning

confidence: 99%

Untitled

2017

Biopolym. Cell

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To identify novel protein partners of translation factor eEF1Bβ in nucleus of human lung carcinoma cells. Methods. Protein partners of eEF1Bβ in the nuclear fraction of A549 cells were identified by co-immunoprecipitation (co-IP) combined with liquid chromatographytandem mass spectrometry (LC-MS/MS). Specific protein partners of eEF1Bβ were further selected by using the results of previously published global, quantitative and dynamic mapping of protein subcellular localization with help of "Mapofthecell" program. Results. 104 highscored proteins interacting with eEF1Bβ in the nuclear fraction of A549 cells have been identified by mass-spectrometry. Among these proteins, 9 partners of eEF1Bβ were confirmed by the co-fractionation approach. Functional analysis of the partners has divided them on the pro-oncogenic (lung-cancer related) and neutral/anti-oncogenic moieties. These two groups are estimated to be spatially separated in human cancer cells. Conclusions. The position of eEF1Bβ as a link between the oncogenic and neutral/tumor-suppressor moieties of its protein partners in nucleus of lung cancer cells is suggested. Deciphering of a possible role of the eEF1Bβ distribution between the pro-cancer or anti-cancer communities of its protein partners can be a subject of further research.

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From Proteomic Analysis to Potential Therapeutic Targets: Functional Profile of Two Lung Cancer Cell Lines, A549 and SW900, Widely Studied in Pre-Clinical Research

Cited by 45 publications

References 96 publications

Characterizing a focused landscape of familial acute respiratory distress syndrome

Characterizing a focused landscape of familial acute respiratory distress syndrome

Cryptotanshinone inhibits lung cancer invasion via microRNA‑133a/matrix metalloproteinase 14 regulation

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