Epithelial-to-mesenchymal transition and EGFR status in NSCLC: the role of vimentin expression

Bronte, Giuseppe; Puccetti, Maurizio; Crinò, Lucio; Bravaccini, Sara

doi:10.1093/annonc/mdy548

Cited by 10 publications

(3 citation statements)

References 5 publications

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“…Vimentin, a key marker of EMT, is closely associated with the malignant phenotype of lung cancer. [ 40 , 41 ] Kaplan–Meier plot analysis revealed that high vimentin expression was associated with shortened survival time in patients with LUAD (Figure S7A,B , Supporting Information) and that there were higher levels of vimentin‐K104Ac in the serum of patients with early‐stage LUAD than those in healthy individuals (Figure S7C , Supporting Information). This evidence suggests that vimentin‐K104Ac may be an important factor that promotes vimentin stability in LUAD.…”

Section: Resultsmentioning

confidence: 99%

The NLRP11 Protein Bridges the Histone Lysine Acetyltransferase KAT7 to Acetylate Vimentin in the Early Stage of Lung Adenocarcinoma

et al. 2023

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Accumulation of vimentin is the core event in epithelial–mesenchymal transition (EMT). Post‐translational modifications have been widely reported to play crucial roles in imparting different properties and functions to vimentin. Here, a novel modification of vimentin, acetylated at Lys104 (vimentin‐K104Ac) is identified, which is stable in lung adenocarcinoma (LUAD) cells. Mechanistically, NACHT, LRR, and PYD domain‐containing protein 11 (NLRP11), a regulator of the inflammatory response, bind to vimentin and promote vimentin‐K104Ac expression, which is highly expressed in the early stages of LUAD and frequently appears in vimentin‐positive LUAD tissues. In addition, it is observed that an acetyltransferase, lysine acetyltransferase 7 (KAT7), which binds to NLRP11 and vimentin, directly mediates the acetylation of vimentin at Lys104 and that the cytoplasmic localization of KAT7 can be induced by NLRP11. Malignant promotion mediated by transfection with vimentin‐K104Q is noticeably greater than that mediated by transfection with vimentin‐WT. Further, suppressing the effects of NLRP11 and KAT7 on vimentin noticeably inhibited the malignant behavior of vimentin‐positive LUAD in vivo and in vitro. In summary, these findings have established a relationship between inflammation and EMT, which is reflected via KAT7‐mediated acetylation of vimentin at Lys104 dependent on NLRP11.

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Section: Resultsmentioning

confidence: 99%

The NLRP11 Protein Bridges the Histone Lysine Acetyltransferase KAT7 to Acetylate Vimentin in the Early Stage of Lung Adenocarcinoma

et al. 2023

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“…While during EMT, the expression of epithelial markers (E-cadherin) decreased, interstitial markers (N-cadherin and vimentin) increased in cancer tissues ( 36 , 37 ). EMT is observed in the invasion and metastasis of many malignant tumors, including NSCLC ( 38 ). In this study, miR-137 suppressed the migration and invasion of NSCLC cells by inhibiting vimentin and promoting E-cadherin.…”

Section: Discussionmentioning

confidence: 99%

miR-137 represses migration and cell motility by targeting COX-2 in non-small cell lung cancer

Luo

Wang

et al. 2022

Transl Cancer Res TCR

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Background: Lung cancer is a common malignant tumor, with, non-small cell lung cancer (NSCLC) accounting for about 80-85% of cases. This study investigated the expression of miR-137 in NSCLC tissues and cells and its effects on the migration and invasion of NSCLC cells and related mechanisms. Methods:We collected the neoplastic and paracancerous tissues of NSCLC patients, detected the expression of miR-137 in NSCLC tissues and cell lines by real-time quantitative polymerase chain reaction (RT-qPCR), and analyzed the correlation between miR-137 expression and the clinicopathological features and survival of NSCLC. Following transfection with miR-137 mimic or inhibitor in NSCLC cell lines (A549 or H1299) to upregulate or downregulate the expression of miR-137, transwell assay was employed to detect the effects of miR-137 on migration or invasion. Online software was employed to predict and analyze the target gene of miR-137, and luciferase reporter gene system was adopted to validate it. The effects of miR-137 on the expressions of COX-2 and Epithelial-Mesenchymal Transition (EMT) related proteins were investigated by Western blot.Results: Compared to paracancerous tissues and BEAS-2B cells, the expressions of miR-137 in NSCLC tissues, A549 and H1299 cells were dramatically down-regulated (P<0.01). After transfection with miR-137 mimic or inhibitor in A549 and H1299 cells, the miR-137 expressions were markedly up-regulated or downregulated (P<0.01), respectively. The number of migrating or invading cells was observably decreased or increased (P<0.01) after transfected with mimic or inhibitor, respectively, while relative luciferase activity was evidently decreased in cells co-transfected with miR-137 mimic and wild type recombined vector of 3'UTR of COX-2. While the expressions of COX-2 and E-cadherin were both substantially reduced in A549 cells treated with miR-137 mimic, that of vimentin was substantially raised. The expression of miR-137 correlated with smoking history, lymph node metastasis, and TNM clinical stage, and patients with high miR-137 expression had apparent longer survival. Conclusions:The expression of miR-137 was significantly down-regulated in NSCLC tissues and cells, and correlated with NSCLC progress. miR-137 suppressed the migration and invasion of NSCLC cells through regulating EMT relative proteins by targeting COX-2. miR-137 is expected to become a novel biomarker and therapeutic target of NSCLC.

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“…During EMT, cancer cells overexpress mesenchymal-related proteins, such as N-cadherin, vimentin, and matrix metallo-proteases (MMP), which enable them to migrate [7,8]. Vimentin, a hallmark of mesenchymal-like conversion of epithelial cells, is overexpressed in NSCLC, which is associated with poor prognosis [9]. In contrast, high levels of E-cadherin diminish the number of cancer stem cells and decrease xenograft tumor growth in A549 cells [10].…”

Section: Introductionmentioning

confidence: 99%

A Novel Anticancer Peptide Derived from Bryopsis plumosa Regulates Proliferation and Invasion in Non-Small Cell Lung Cancer Cells

Kim,

Jung

et al. 2023

Marine Drugs

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The discovery of new highly effective anticancer drugs with few side effects is a challenge for drug development research. Natural or synthetic anticancer peptides (ACPs) represent a new generation of anticancer agents with high selectivity and specificity. The rapid emergence of chemoradiation-resistant lung cancer has necessitated the discovery of novel anticancer agents as alternatives to conventional therapeutics. In this study, we synthesized a peptide containing 22 amino acids and characterized it as a novel ACP (MP06) derived from green sea algae, Bryopsis plumosa. Using the ACP database, MP06 was predicted to possess an alpha-helical secondary structure and functionality. The anti-proliferative and apoptotic effects of the MP06, determined using the cytotoxicity assay and Annexin V/propidium iodide staining kit, were significantly higher in non-small-cell lung cancer (NSCLC) cells than in non-cancerous lung cells. We confirmed that MP06 suppressed cellular migration and invasion and inhibited the expression of N-cadherin and vimentin, the markers of epithelial–mesenchymal transition. Moreover, MP06 effectively reduced the metastasis of tumor xenografts in zebrafish embryos. In conclusion, we suggest considering MP06 as a novel candidate for the development of new anticancer drugs functioning via the ERK signaling pathway.

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Epithelial-to-mesenchymal transition and EGFR status in NSCLC: the role of vimentin expression

Cited by 10 publications

References 5 publications

The NLRP11 Protein Bridges the Histone Lysine Acetyltransferase KAT7 to Acetylate Vimentin in the Early Stage of Lung Adenocarcinoma

The NLRP11 Protein Bridges the Histone Lysine Acetyltransferase KAT7 to Acetylate Vimentin in the Early Stage of Lung Adenocarcinoma

miR-137 represses migration and cell motility by targeting COX-2 in non-small cell lung cancer

A Novel Anticancer Peptide Derived from Bryopsis plumosa Regulates Proliferation and Invasion in Non-Small Cell Lung Cancer Cells

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