Keratin 18 induces proliferation, migration, and invasion in gastric cancer via the MAPK signalling pathway

Wang, Peng-Bin; Chen, Yan; Ding, Guang-Rong; Du, Hong-Wei; Fan, H. Christina

doi:10.1111/1440-1681.13401

Cited by 18 publications

(16 citation statements)

References 18 publications

(49 reference statements)

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“… 2020 ; Wang et al. 2021 ). As one of the most important MAPK family pathways, JNK is mainly involved in stress response, apoptosis, and other physiological processes.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Elian granules in the treatment of precancerous lesions of gastric cancer in rats through the MAPK signalling pathway based on network pharmacology

Jia

Lin

et al. 2021

Pharmaceutical Biology

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Context Elian Granules have been applied in the treatment of precancerous lesions of gastric cancer (PLGC) and achieved good results. However, its exact mechanism remains unclear. Objectives To explore the mechanism of Elian granules in treating PLGC through the mitogen-activated protein kinase (MAPK) signalling pathway based on network pharmacology. Materials and methods Through network pharmacological methods, the targets of the active component of Elian granules against PLGC were obtained. Subsequently, Specific Pathogen Free (SPF) male Sprague Dawley (SD) rats were randomly divided into normal, model, and Elian granule groups. The N -methyl- N ′-nitro- N -nitrosoguanidine comprehensive method was used to establish the PLGC rat model. The model and Elian granule groups were given normal saline and Elian granule aqueous solution (3.24 g/kg/d) intragastric administration, respectively, for 24 weeks. The pathological changes in gastric tissues were observed by hematoxylin-eosin staining. The protein expression of p-JNK and p-p38 was verified by western blotting. Results 394 and 4,395 targets were identified in Elian granules and PLGC, respectively. The 190 common targets were mainly enriched in MAPK signalling pathways. The gastric mucosal epithelium was still intact, the glands were arranged regularly, and no goblet cells or apparent inflammatory cell infiltration were observed in the Elian granule group. The expression of p-JNK and p-p38 protein of the Elian granule group (0.83 ± 0.08; 1.18 ± 0.40) was significantly higher than the model group (0.27 ± 0.14; 0.63 ± 0.14) ( p < 0.01; p < 0.05). Discussion and conclusions Elian granules may play a critical role in the treatment of rat PLGC by up-regulating the expression of p-JNK and p-p38 proteins in the MAPK signalling pathway, thus providing a scientific basis for clinical application.

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“… 2020 ; Wang et al. 2021 ). As one of the most important MAPK family pathways, JNK is mainly involved in stress response, apoptosis, and other physiological processes.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Elian granules in the treatment of precancerous lesions of gastric cancer in rats through the MAPK signalling pathway based on network pharmacology

Jia

Lin

et al. 2021

Pharmaceutical Biology

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“…And based on network system biology we select one target KRT18 associated with poor prognosis in PanC. KRT18 could induce proliferation, migration, and invasion via MAKP signaling in gastric cancer ( Wang et al, 2020 ). However, the mechanism by which KRT18 contributes to PanC has not been determined and should be a focus of further research.…”

Section: Discussionmentioning

confidence: 99%

Identification of Novel Metabolism-Associated Subtypes for Pancreatic Cancer to Establish an Eighteen-Gene Risk Prediction Model

Gao

Zhang

Fei

et al. 2021

Front. Cell Dev. Biol.

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Pancreatic cancer (PanC) is an intractable malignancy with a high mortality. Metabolic processes contribute to cancer progression and therapeutic responses, and histopathological subtypes are insufficient for determining prognosis and treatment strategies. In this study, PanC subtypes based on metabolism-related genes were identified and further utilized to construct a prognostic model. Using a cohort of 171 patients from The Cancer Genome Atlas (TCGA) database, transcriptome data, simple nucleotide variants (SNV), and clinical information were analyzed. We divided patients with PanC into metabolic gene-enriched and metabolic gene-desert subtypes. The metabolic gene-enriched subgroup is a high-risk subtype with worse outcomes and a higher frequency of SNVs, especially in KRAS. After further characterizing the subtypes, we constructed a risk score algorithm involving multiple genes (i.e., NEU2, GMPS, PRIM2, PNPT1, LDHA, INPP4B, DPYD, PYGL, CA12, DHRS9, SULT1E1, ENPP2, PDE1C, TPH1, CHST12, POLR3GL, DNMT3A, and PGS1). We verified the reproducibility and reliability of the risk score using three validation cohorts (i.e., independent datasets from TCGA, Gene Expression Omnibus, and Ensemble databases). Finally, drug prediction was completed using a ridge regression model, yielding nine candidate drugs for high-risk patients. These findings support the classification of PanC into two metabolic subtypes and further suggest that the metabolic gene-enriched subgroup is associated with worse outcomes. The newly established risk model for prognosis and therapeutic responses may improve outcomes in patients with PanC.

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“…According to the histologic criteria of CNS WHO (2016), (33). The full-length fragment of KRT18 has been proposed to be used as a biomarker of liver damage (34).…”

Section: Discussionmentioning

confidence: 99%

Integrated genomic and transcriptomic analysis suggests KRT18 mutation and MTAP are key genetic alterations related to the prognosis between astrocytoma and glioblastoma

Li¹,

Jin²,

Zou³

et al. 2021

Ann Transl Med

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Background: Astrocytoma and glioblastoma (GBM) are the two main subtypes of glioma, with the 2016 World Health Organization Classification of Tumors of the Central Nervous System (CNS WHO) classifying them into different grades. GBM is the most malignant among all CNS tumors with a 5-year survival rate of less than 5%. Although the prognosis of patients with astrocytoma is better than that of GBM in general, patients with anaplastic astrocytoma (AA) and isocitrate dehydrogenase (IDH) wild type have a similar prognosis as GBM and entail a high risk of progression. Exploring the molecular driving force behind the malignant phenotype of astrocytoma and GBM will help explain the diversity of glioma and discover new drug targets.Methods: We enrolled 12 patients with astrocytoma and 12 patients with GBM and performed wholeexome sequencing (WES) and RNA sequencing analysis on tumor samples from the patients. Results:We found that the somatic mutation of KRT18, which is associated with cell apoptosis and adhesion by interacting with receptor 1-associated protein (TRADD) and pinin, was significantly enriched in astrocytoma, but rare in GBM. Copy number loss of MTAP, which is closely related to a poor prognosis of glioma, was found to be significantly enriched in GBM. In addition, different somatic copy number alteration (SCNA), gene expression, and immune cell infiltration patterns between astrocytoma and GBM were found.Conclusions: This study revealed the distinct characteristics of astrocytoma and GBM at the DNA and RNA level. Somatic mutation of KRT18 and copy number loss of MTAP, two key genetic alterative genes in astrocytoma and GBM, have the potential to become therapeutic targets in glioma.

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Keratin 18 induces proliferation, migration, and invasion in gastric cancer via the MAPK signalling pathway

Cited by 18 publications

References 18 publications

Mechanism of Elian granules in the treatment of precancerous lesions of gastric cancer in rats through the MAPK signalling pathway based on network pharmacology

Mechanism of Elian granules in the treatment of precancerous lesions of gastric cancer in rats through the MAPK signalling pathway based on network pharmacology

Identification of Novel Metabolism-Associated Subtypes for Pancreatic Cancer to Establish an Eighteen-Gene Risk Prediction Model

Integrated genomic and transcriptomic analysis suggests KRT18 mutation and MTAP are key genetic alterations related to the prognosis between astrocytoma and glioblastoma

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