Keratin 17 Promotes Lung Adenocarcinoma Progression by Enhancing Cell Proliferation and Invasion

Li, Jianbo; Liu, Lei; Cao, Lina; Wen, Qiang

doi:10.12659/msm.909350

Cited by 40 publications

(38 citation statements)

References 34 publications

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“…Of note, LAC and SCC account for 50% and 30%, respectively (Larrayoz et al, ). Despite the remarkable advances in diagnosis and therapeutic technology, the 5‐year survival rate for NSCLC patients is still approximately 15% (Miller, ; Liu et al, ; Men et al, ). Therefore, better understanding of the cellular and molecular changes in lung cancer is essential.…”

Section: Introductionmentioning

confidence: 99%

TCF19 contributes to cell proliferation of non‐small cell lung cancer by inhibiting FOXO1

Zhou

Chen

Deng

et al. 2019

Cell Biology International

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Transcription factor 19 (TCF19) harbors a forkhead association (FHA) domain, a proline-rich region, a PHD or RING finger region, suggesting that TCF19 possesses a powerful function. However, its expression and function remains unknown in non-small-cell lung cancer (NSCLC). The function cluster analysis was carried out using Metascape website. 3-(4,5-Dimethyl-2-thiazolyl)2,5-diphenyl-2H-tetrazolium bromide (MTT), colony formation, and anchorage-independent growth ability assay were carried out to detect the effect of TCF19 on cell proliferation. Bromodeoxyuridine (Brdu) labeling and flow cytometry assay were used to evaluate the effect of TCF19 on cell-cycle progression. Quantitative polymerase chain reaction and chromatin immunoprecipitation assay were performed to investigate the mechanism by which TCF19 is involved in cell-cycle transition. By analyzing the publicly available dataset, The Cancer Genome Atlas (TCGA), we found that TCF19 is significantly increased in the lung adenocarcinoma (LAC) and squamous cell carcinoma (SCC), two primary histological subtype of NSCLC. Besides, further function cluster analysis exhibited that TCF19 may mainly participate in cell cycle. MTT, colony formation, and anchorage-independent growth ability assay confirmed that overexpression of TCF19 enhances the proliferation of both LAC and SCC cells. Besides, further experiments revealed that TCF19 contributes to cell cycle G1/S transition. Not only that, upregulation of TCF19 can inhibit the expression of p21, p27, and p57, while promote the expression of cyclin D1 by inhibiting FOXO1. Our research offers important evidence that TCF19 can promote cell-cycle progression of NSCLC cells, and TCF19 may served as novel therapeutic targets.

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Section: Introductionmentioning

confidence: 99%

TCF19 contributes to cell proliferation of non‐small cell lung cancer by inhibiting FOXO1

Zhou

Chen

Deng

et al. 2019

Cell Biology International

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“…4C, bottom); for example, NFKBIA (IκBα) is a pan-cancer tumor 20 suppressor via inhibition of pro-tumoral NFκB signaling (54), overexpression of ID3 inhibits tumor cell migration and invasion in vitro and in similar xenograft models of lung adenocarcinoma xenograft (55), and downregulation of ASS1 supports tumor metabolism and proliferation (56). Paradoxically, our most significant negative hit is KRT17, which has previously been implicated in promoting invasiveness in lung adenocarcinoma (57) and its overexpression is associated with poor prognosis in many cancers (58). This suggests that KRT17 may play a context-specific role in metastatic progression in this model, which could be further explored experimentally.…”

Section: Transcriptional Signatures Of Distinct Metastatic Phenotypesmentioning

confidence: 77%

Single-cell lineages reveal the rates, routes, and drivers of metastasis in cancer xenografts

Quinn

Jones

Okimoto

et al. 2020

Preprint

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N.Y.).One Sentence Summary: Detailed single-cell phylogenies capture the frequency, tissue routes, and seeding patterns of metastasis in vivo. Abstract:25 2 Consequential events in cancer progression are typically rare and occur in the unobserved past. Detailed cell phylogenies can capture the history and chronology of such transient events -including metastasis. Here, we applied our Cas9-based lineage tracer to study metastatic progression in a lung cancer xenograft mouse model, revealing the underlying rates, routes, and patterns of metastasis. We report deeply resolved phylogenies for tens of thousands of metastatically disseminated cancer cells. We observe surprisingly diverse metastatic phenotypes, 5 ranging from metastasis-incompetent to highly aggressive populations, and these differences are associated with characteristic changes in transcriptional state, including differential expression of metastasis-related genes like IFI27 and ID3. We further show that metastases transit via tissue routes that are diverse, complex, and multidirectional, and identify examples of reseeding, seeding cascades, and parallel seeding topologies. More broadly, we demonstrate the power of next-generation lineage tracers to record cancer evolution at high resolution 10 and vast scale. Main Text:Cancer progression is governed by evolutionary principles (reviewed in (1)), which leave clear phylogenetic signatures upon every step of this process (2, 3), from early acquisition of oncogenic mutations (i.e., the relationships between normal and malignantly transformed cells (4)), to metastatic colonization of distant 15 tissues (i.e., the relationship between the primary tumor and metastases (5)), and finally adaptation to therapeutic challenges (i.e., the relationship between sensitive and resistant clones (6)). Metastasis is a particularly important step in cancer progression to study because it is chiefly responsible for disease relapse and mortality (7). Yet because metastatic events are intrinsically rare, transient, and stochastic (8,9), they are challenging to monitor in real time. Analogous to the cell fate maps that have played an essential role in deepening our understanding of 20 organismal development and cell type differentiation (10, 11), accurately reconstructed phylogenetic trees of tumors and metastases can reveal key features of this process, such as the clonality, timing, frequency, origins, and destinations of metastatic seeding (12).Lineage tracing techniques allow one to map the genealogy of related cells, providing a critical tool for exploring the phylogenetic principles of biological processes like cancer progression and metastasis. Classical

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“…According to Balabko et al (2014) RORC is a specific transcription factor in the tumor area of lung tissue in patients with LUAD. DLX5 (Kato et al, 2008;Balabko et al, 2014), MUC1 (Mashima et al, 2005;Molina-Pinelo et al, 2014), and KRT17 (Erdogan et al, 2009;Liu et al, 2018) were found to be overexpressed in LUAD.…”

Section: The Biological Significance Of the Identified Signaturementioning

confidence: 94%

Integrative Analysis of Methylation and Gene Expression in Lung Adenocarcinoma and Squamous Cell Lung Carcinoma

Zhang

Zhou

Cheng³

et al. 2020

Front. Bioeng. Biotechnol.

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Lung cancer is a highly prevalent type of cancer with a poor 5-year survival rate of about 4-17%. Eighty percent lung cancer belongs to non-small-cell lung cancer (NSCLC). For a long time, the treatment of NSCLC has been mostly guided by tumor stage, and there has been no significant difference between the therapy strategy of lung adenocarcinoma (LUAD) and squamous cell lung carcinoma (SCLC), the two major subtypes of NSCLC. In recent years, important molecular differences between LUAD and SCLC are increasingly identified, indicating that targeted therapy will be more and more histologically specific in the future. To investigate the LUAD and SCLC difference on multi-omics scale, we analyzed the methylation and gene expression data together. With the Boruta method to remove irrelevant features and the MCFS (Monte Carlo Feature Selection) method to identify the significantly important features, we identified 113 key methylation features and 23 key gene expression features. HNF1B and TP63 were found to be dysfunctional on both methylation and gene expression levels. The experimentally determined interaction network suggested that TP63 may play an important role in connecting methylation genes and expression genes. Many of the discovered signature genes have been supported by literature. Our results may provide directions of precision diagnosis and therapy of LUAD and SCLC.

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Keratin 17 Promotes Lung Adenocarcinoma Progression by Enhancing Cell Proliferation and Invasion

Cited by 40 publications

References 34 publications

TCF19 contributes to cell proliferation of non‐small cell lung cancer by inhibiting FOXO1

TCF19 contributes to cell proliferation of non‐small cell lung cancer by inhibiting FOXO1

Single-cell lineages reveal the rates, routes, and drivers of metastasis in cancer xenografts

Integrative Analysis of Methylation and Gene Expression in Lung Adenocarcinoma and Squamous Cell Lung Carcinoma

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