COL4A1 promotes the proliferation and migration of oral squamous cell carcinoma cells by binding to NID1

Tian, Xiaobei; Sun, Jian; Li, Changshun; Zhang, Kun

doi:10.3892/etm.2023.11875

Cited by 8 publications

(3 citation statements)

References 43 publications

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“…Moreover, upregulation of COL4A1 has been reported in patients with Oral Squamous Cell Carcinoma. [ 34 ] Elevated levels of COL4A1 contribute to enhanced migration, invasion, and proliferation in various cancers, including breast cancer and bladder cancer. Prior investigations have also recognized COL4A1 as a pivotal gene implicated in the initiation, advancement, and recurrence of gastric cancer, [ 35 ] and have associated its overexpression with unfavorable prognosis.…”

Section: Discussionmentioning

confidence: 99%

A pan-cancer analysis of TNFAIP8L1 in human tumors

Sun,

Zhang,

Zhu

et al. 2023

Medicine

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TNFAIP8L1, as a recently identified member in TNFAIP8 family, plays an important role in tumorigenesis. However, a pan-cancer analysis of TNFAIP8L1 in human tumors has not been conducted until now. The main purpose of study is to investigate TNFAIP8L1 during 33 different types of human tumors by using TCGA and GTEx. The pan-cancer analysis showed that TNFAIP8L1 was significantly over-expressed in 15 cancers and low-expressed in 9 cancers. There were distinct relations between TNFAIP8L1 expression and prognosis of patients with cancer. Furthermore, we also found that DNA methylation and RNA modification of TNFAIP8L1 were associated with many cancers. And then, we detected that TNFAIP8L1 level was positively associated with cancer-associated fibroblasts (CAFs) in many tumors. And, we obtained that TNFAIP8L1 expression was related with most of immune inhibitory and stimulatory genes in multiple types of tumors. We also found TNFAIP8L1 expression was correlated with most of chemokine, receptor, MHC, immunoinhibitor and immunostimulator gens in most of cancers. Moreover, we detected TNFAIP8L1 expression was associated with TMB and MSI in several tumors. Finally, TNFAIP8L1 gene had a significant positive association with 5 genes including BCL6B, DLL4, PCDH12, COL4A1 and DLL4 in the majority of tumors. GO enrichment and KEGG pathway analyses showed that TNFAIP8L1 in thepathogenesis of cancer may be related to “purine nucleoside binding,” “purine ribonucleoside binding,” “ECM-receptor interaction,” etc. Our first pan-cancer study may provide a deep comprehending of TNFAIP8L1 in tumoeigenesis from different tumors.

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Section: Discussionmentioning

confidence: 99%

A pan-cancer analysis of TNFAIP8L1 in human tumors

Sun,

Zhang,

Zhu

et al. 2023

Medicine

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“…High expression of COL4A1 can promote the proliferation of colon tumor cells and may be a target to inhibit the proliferation of colon tumor cells.However, the mechanism by which COL4A1 inhibits tumor cell proliferation remains unclear.Nidogen-1(NID1) is a component of the extracellular matrix and the basement membrane [40].The main function of NID1 is to provide a link between laminin, collagen, proteoglycans and cell surface receptors to control cell polarization, migration and invasion [41]. Tian et al showed that COL4A1 promotes the proliferation of oral squamous cell carcinoma by binding to NID1 [42].…”

Section: Disscussionmentioning

confidence: 99%

Overexpression of COL4A1 promotes progression of colon cancer and is associated with poor prognosis

Li,

Wang,

Wang

2024

Preprint

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Background Colon cancer is one of the common malignant tumor diseases of the digestive system, and its incidence and mortality rate are increasing year by year.Collagen type IV alpha 1 chain (COL4A1) is a hypoxia-associated gene (a collagen family protein) involved in the formation of the extracellular matrix.COL41 plays an important role in the progression of several cancers and is associated with poorer prognostic outcomes.However, whether it can mediate the progression of colon cancer is unclear. Method First, based on the TCGA-COAD dataset, we analyzed the mRNA expression levels of COL4A1 in colon cancer and evaluated the relationship between COL4A1 and clinicopathological features as well as prognosis.Then,we further analyzed the expression of COL4A1 in colon cancer tissues and colon tumor cells by qRT-PCR and HIC.Colon cancer cell lines SW480 and HCT116 were transfected with small interfering rna (siRNA) to construct low expression cell lines.Clone formation assay and transwell migration and invasion assays were used to detect the effects of knockdown of COL4A1 on proliferation, migration and invasion of colon cancer cells. Result Bioinformatics analysis showed that COL4A1 was significantly higher expressed in colon cancer tissues than in normal colon tissues. High expression of COL4A1 is associated with poor clinical stage and poor prognosis.We observed that COL4A1 was also highly expressed in colon cancer tissue and colon tumor cells compared with normal colon tissue and normal colon cells.Downregulation of COL4A1 significantly inhibited tumor cell proliferation, migration and invasion progression. Conclusion In summary, our study suggests that COL4A1 is a potential oncogene for colon cancer and can mediate colon cancer progression.

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“…Immunostaining showed that the localization of MMP14 is also p turbed by TKS4 deletion, as the protein was more precisely located around the nucleu the TKS4 KO cells, with a decreased protein level compared to MMP14 observed in spindles (invadopodia and podosome) of WT cells (Supplementary Figure S8). According to the transcriptomic analysis, a noticeable elevation could be observed in the expression of most of the invasion marker genes (Figures 3B and S3B), such as urokinase-type plasminogen activator (PLAU) [65], laminin genes (LAMA3, LAMA5) [66][67][68], collagen-related genes (COL1A1, COL4A3, and COL6A2) [69][70][71][72], cathepsin genes (CTSA, CTSB) [73][74][75], serpine1 (PAI-1) [76], MMP genes (MMP7, 9, 13, 14, and 17) [77][78][79][80][81], and integrin-related genes (ITGA2, ITGA3, and ITGB4) [82][83][84]. The analysis also revealed that over 85% of recognized invasion markers undergo alterations upon TKS4 deletion, and around 75% of these changes are reversed by the inhibition of EZH2 activity (Figure 3C and Supplementary Tables S1A and S2).…”

Section: Absence Of Tks4 Induces Invasion Through Ezh2 Hyperactivitymentioning

confidence: 99%

Morphological Changes Induced by TKS4 Deficiency Can Be Reversed by EZH2 Inhibition in Colorectal Carcinoma Cells

Jacksi,

Schad,

Tantos

2024

Biomolecules

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Background: The scaffold protein tyrosine kinase substrate 4 (TKS4) undergoes tyrosine phosphorylation by the epidermal growth factor receptor (EGFR) pathway via Src kinase. The TKS4 deficiency in humans is responsible for the manifestation of a genetic disorder known as Frank–Ter Haar syndrome (FTHS). Based on our earlier investigation, the absence of TKS4 triggers migration, invasion, and epithelial–mesenchymal transition (EMT)-like phenomena while concurrently suppressing cell proliferation in HCT116 colorectal carcinoma cells. This indicates that TKS4 may play a unique role in the progression of cancer. In this study, we demonstrated that the enhancer of zeste homolog 2 (EZH2) and the histone methyltransferase of polycomb repressive complex 2 (PRC2) are involved in the migration, invasion, and EMT-like changes in TKS4-deficient cells (KO). EZH2 is responsible for the maintenance of the trimethylated lysine 27 on histone H3 (H3K27me3). Methods: We performed transcriptome sequencing, chromatin immunoprecipitation, protein and RNA quantitative studies, cell mobility, invasion, and proliferation studies combined with/without the EZH2 activity inhibitor 3-deazanoplanocine (DZNep). Results: We detected an elevation of global H3K27me3 levels in the TKS4 KO cells, which could be reduced with treatment with DZNep, an EZH2 inhibitor. Inhibition of EZH2 activity reversed the phenotypic effects of the knockout of TKS4, reducing the migration speed and wound healing capacity of the cells as well as decreasing the invasion capacity, while the decrease in cell proliferation became stronger. In addition, inhibition of EZH2 activity also reversed most epithelial and mesenchymal markers. We investigated the wider impact of TKS4 deletion on the gene expression profile of colorectal cancer cells using transcriptome sequencing of wild-type and TKS4 knockout cells, particularly before and after treatment with DZNep. Additionally, we observed changes in the expression of several protein-coding genes and long non-coding RNAs that showed a recovery in expression levels following EZH2 inhibition. Conclusions: Our results indicate that the removal of TKS4 causes a notable disruption in the gene expression pattern, leading to the disruption of several signal transduction pathways. Inhibiting the activity of EZH2 can restore most of these transcriptomics and phenotypic effects in colorectal carcinoma cells.

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COL4A1 promotes the proliferation and migration of oral squamous cell carcinoma cells by binding to NID1

Cited by 8 publications

References 43 publications

A pan-cancer analysis of TNFAIP8L1 in human tumors

A pan-cancer analysis of TNFAIP8L1 in human tumors

Overexpression of COL4A1 promotes progression of colon cancer and is associated with poor prognosis

Morphological Changes Induced by TKS4 Deficiency Can Be Reversed by EZH2 Inhibition in Colorectal Carcinoma Cells

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