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Smoking promotes the progression of colorectal cancer via CKAP2L/STAT3/AREG/EGFR axis

ABSTRACT: Smoking is a major risk factor for colorectal cancer (CRC). But the underlying molecular mechanisms by which smoking promotes CRC remain unclear. The positive association between smoking and CRC was confirmed by both cross-sectional study and mendelian randomization analyses. RNA-seq sequencing and bioinformatics analysis were conducted to identify the key genes involved in smoking-induced CRC progression. After treatment with cigarette smoke extract in CRC cells, cell proliferation and metastasis were enhanced. Subsequently, cytoskeleton associated protein 2 like (CKAP2L) was identified as a key gene involved in smoking-induced CRC and its downregulation inhibited cell proliferation and metastasis. CKAP2L is an important part of the cell centrosome and serves a critical role in spindle formation. Previous studies have demonstrated that CKAP2L mediates the cell cycle in a variety of cancer types, promoting the progression and spread of tumors.A recent study reported that regulatory factor X5-regulated CKAP2L can promote the proliferation and metastasis of CRC cells. In this study, we upregulated CKAP2L in HCT116 cells and downregulated CKAP2L in RKO cells. Then, these cells were subjected to the RNA-seq to explore the expression of relative genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE305020 | GEO | 2026/01/20

REPOSITORIES: GEO

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Smoking promotes the progression of colorectal cancer via CKAP2L/STAT3/AREG/EGFR axis

Project description:Smoking is a major risk factor for colorectal cancer (CRC). But the underlying molecular mechanisms by which smoking promotes CRC remain unclear. The positive association between smoking and CRC was confirmed by both cross-sectional study and mendelian randomization analyses. RNA-seq sequencing and bioinformatics analysis were conducted to identify the key genes involved in smoking-induced CRC progression. After treatment with cigarette smoke extract (CSE) in CRC cells, cell proliferation and metastasis were enhanced. Subsequently, we isolated the total RNA of HCT116 cells treated with CSE and subjected it to the RNA-seq to explore the differentially expressed genes.

2026-01-20 | GSE305039 | GEO

Epigenomic analysis reveals a unique DNA methylation program of metastasis-competent circulating tumor cells in colorectal cancer

Project description:Metastasis is the main cause of cancer-related deaths in patients with solid tumors, including colorectal cancer (CRC). Circulating tumor cells (CTCs) and epigenetic alterations are involved in the development of metastasis. It is important to characterize the DNA methylation pattern of metastasis-competent CTCs to better understand the metastatic process and obtain new clinical applications for cancer patients. Therefore, the aim of this study was to investigate the DNA methylation landscape of metastasis-competent CTCs in CRC. The DNA methylome of the human colorectal cancer-derived cell line CTC-MCC-41 was compared with primary (HT29, Caco2, HCT116, RKO) and metastatic (SW620 and COLO205) CRC cells using a genome-wide methylation analysis.

2023-09-20 | GSE220096 | GEO

Genetic Architecture of Smoking and Smoking Cessation

Project description:Genetic Architecture of Smoking and Smoking Cessation

| PRJNA75689 | ENA

Gene Expression Circulating B Lymphocytes for Smoking Females

Project description:B cells were found to be directly associated with the onset and development of many smoking-induced diseases. However, the in vivo molecular response of B cells underlying the female cigarette smoking remains unknown. Using the genome-wide Affymetrix HG-133A GeneChip® microarray, we compared the gene expression profiles of peripheral circulating B cells between 39 smoking and 40 non-smoking healthy US white females.

2009-12-25 | GSE18723 | GEO

Proteomic analysis upon miR195/497 replacement reveals potential chemo sensitizing candidates for colorectal cancer

Project description:Patients with advanced colorectal cancer (CRC) are commonly treated with systemic combination therapy but suffer eventually from drug resistance. MicroRNAs (miRNAs) are suggested to play a role in treatment resistance of CRC. We studied whether restoring downregulated miR-195-5p and 497-5p sensitize CRC cells to currently used chemotherapeutics 5-fluorouracil, oxaliplatin and irinotecan. Sensitivity to 5-FU, oxaliplatin and irinotecan before and after transfection with miR-195-5p and miR-497-5p mimics was analyzed in CRC cell lines HCT116, RKO, DLD-1 and SW480. Mass spectrometry based proteomic analysis of transfected and wild-type cells was used to identify targets involved in sensitivity to chemotherapy. Proteomic analysis revealed 181 proteins with significantly altered expression after transfection with miR-195-5p mimic in HCT116 and RKO, including 118 downregulated and 63 upregulated proteins. After transfection with miR-497-5p mimic, 130 proteins were significantly downregulated and 102 were upregulated in HCT116 and RKO (P<0.05 and FC<-3 or FC>3). CHUK and LUZP1 were coinciding downregulated proteins in sensitized CRC cells after transfection with either mimic. Resistance mechanisms of these two proteins may be related to nuclear factor kappa-B signaling and G1 cell cycle arrest, respectively. Restoring miR-195-5p and miR-497-5p expression enhanced sensitivity to chemotherapy, mainly oxaliplatin, in CRC cells and could be a promising treatment strategy for patients with mCRC. Proteomics revealed potential targets of these miRNAs involved in sensitivity to chemotherapy.

2019-09-27 | PXD015369 | Pride

Circular RNA hsa_circ_0064559 is identified to affect the progression of colorectal cancer [PrimeView]

Project description:A series of circular RNAs (circRNAs) play a pivotal role in the pathogenesis of CRC.We found that hsa_circ_0064559 knockdown had the most significant reduction in the proliferation of CRC cells. The expressed genes(DEGs) between shEV group (n=3) and shCIRC group (n=3) from RKO cells were analyzed on Affymetrix GeneChip primeview human gene expression array (Affymetrix, CA, USA).

2023-06-14 | GSE226489 | GEO

Persistence of Smoking-induced Dysregulation of Small Airway Epithelium miRNA Expression Despite Smoking Cessation

Project description:Rationale: Even after quitting smoking, the risk of the development of chronic obstructive pulmonary disease (COPD) and lung cancer remains significantly higher compared to never-smokers. Objectives: Based on the knowledge that COPD and most lung cancers start in the small airway epithelium (SAE), we hypothesized that smoking modulates miRNA expression in the SAE linked to the pathogenesis of smoking-induced airway disease, and that some of these changes persist after smoking cessation. Methods: SAE was collected from 10th to 12th order bronchi using fiberoptic bronchoscopy. Affymetrix miRNA 2.0 arrays were used to assess miRNA expression in the SAE from 10 healthy never-smokers and 10 healthy smokers, before and after they quit for 3 months. Smoking status was determined by urine nicotine and cotinine measurement. Results: There were significant differences in the expression of 34 miRNAs between healthy smokers and healthy never-smokers (p<0.01, fold-change >1.5), with functions associated with lung development, airway epithelium differentiation, inflammation and cancer. After quitting smoking for 3 months, 12 out of the 34 miRNAs did not return to normal levels, with Wnt/β-catenin signaling pathway the top enriched pathway of the target genes of the persistent deregulated miRNAs. Conclusions: In the context that many of these persistent smoking-dependent miRNAs are associated with differentiation, inflammation diseases or lung cancer, it is likely that persistent smoking-related changes in small airway epithelium miRNAs play a role in the subsequent development of these disorders.

2015-11-23 | GSE53519 | GEO

RNA-seq of cells with centrosome amplification

Project description:Centrosome amplification induces proliferation arrest and cell invasion. The fate of centrosome amplification cells are studied here.

2021-10-07 | E-MTAB-11126 | biostudies-arrayexpress

Smoking effect on DNA methylation in human blood cell types

Project description:Tobacco smoking alters DNA methylation profiles of immune cells which may underpin some of the pathogenesis of smoking-associated diseases. However, approaches linking smoking-driven epigenetic effects in specific immune cell types with disease risk are limited. We isolated six leukocyte subtypes, CD14+ monocytes, CD15+ granulocytes, CD19+ B cells, CD4+ T cells, CD8+ T cells, and CD56+ natural killer cells, from whole blood of healthy adult smokers and nonsmokers for epigenome-wide association study (EWAS).

2023-06-20 | GSE224807 | GEO

microRNA expression signatures in colorectal cancer cell lines with demethylating treatment

Project description:To screen for epigenetically silenced miRNAs, wecarried out miRNA microarray analysis in three colorectal cancer (CRC) cell lines (HCT116, DLD-1 and RKO) treated with or without 5-aza-2'-deoxycytidine (aza). HCT116 and RKO cells were also treated with aza plus 4-phenylbutyric acid (PBA). In addition, we analyzed HCT116 cells in which the DNA methyltransferase genes DNMT1 and DNMT3B were genetically disrupted (double knockout; DKO cells), thereby abrogating DNA methylation. Expression of a majority of miRNAs was downregulated in all three CRC cell lines tested, as compared to normal colonic mucosa. DAC treatment upregulated expression of a large number of miRNAs in all three CRC cell lines, and combination treatment with DAC plus PBA induced even greater numbers of miRNAs in CRC cells. The most profound effect on the miRNA expression profile was induced by genetic disruption of DNMT1 and DNMT3B in HCT116 cells. CRC cells were treated with 5-aza-2’-deoxycytidine (aza) or aza plus 4-phenylbutyrate (PBA). Nomal colon RNA was purchased from BioChain. Expression of 470 miRNAs was analyzed using Human miRNA Microarray V1 (G4470A; Agilent technologies, Santa Clara, CA, USA).

2011-07-01 | E-GEOD-29900 | biostudies-arrayexpress

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