CALD1 Modulates Gliomas Progression via Facilitating Tumor Angiogenesis

Cheng, Quan; Tang, Anliu; Wang, Zeyu; Fang, Ning; Zhang, Zhuojing; Zhang, Jintao; Li, Chuntao; Zeng, Yu

doi:10.3390/cancers13112705

Cited by 18 publications

(12 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Based on these results, MIR100HG regulates the expression of the CALD1 by targeting miR-142-5p. Caldesmon (CALD1) is a cytoskeletal protein that regulates cell morphology and movement through interactions with actin filaments, and is closely related to tumor cell migration, invasion, metastasis and blood vessel formation (Cheng et al, 2021;Yao et al, 2021). Therefore, it has attracted increasing attention of cancer researcher in recent years.…”

Section: Discussionmentioning

confidence: 99%

MIR100HG Regulates CALD1 Gene Expression by Targeting miR-142-5p to Affect the Progression of Bladder Cancer Cells in vitro, as Revealed by Transcriptome Sequencing

Zhang

Wang

et al. 2022

Front. Mol. Biosci.

View full text Add to dashboard Cite

Background/Aim: The role of long non-coding RNA (lncRNA) and competing endogenous RNAs (ceRNA) networks in bladder cancer, especially the function of lncRNA-miRNA-mRNA regulatory network in bladder cancer, are still relatively poorly understood. This research mainly used transcriptome sequencing to screen key lncRNAs and ceRNAs, explore their pathogenic mechanism in bladder cancer, and search for potential diagnostic and therapeutic targets.Methods: High-throughput transcriptome sequencing, combined with the limma package, Kaplan-Meier curve analysis, lncRNA-mRNA coexpression network, univariate Cox analysis, multivariate Cox analysis, protein-protein interaction (PPI), functional enrichment, weighed gene co-expression network analysis (WGCNA), ceRNA network and quantitative PCR (qPCR) analyses were performed to assess and screen differentially expressed lncRNAs and mRNAs. Then, the effects of MIR100HG on the proliferation, migration and invasion of the bladder cancer cell line 5,637 were evaluated using cell counting kit-8(CCK-8), wound-healing and transwell assays, respectively. A dual luciferase reporter assay was used to validate the MIR100HG/miR-142-5p and miR-142-5p/CALD1 targeting relationship, and the regulatory relationship among MIR100HG/miR-142-5p/CALD1 expression was explored using qPCR and western blot. Results: A total of 127 differentially expressed lncRNAs and 620 differentially expressed mRNAs were screened. Based on the survival prognosis analysis, Cox analysis, lncRNA-mRNA network, PPI network and WGCNA, we obtained 3 key lncRNAs and 13 key mRNAs, as well as the MIR100HG/miR-142-5p/CALD1 key regulatory axis. qPCR results showed that compared with the adjacent tissues, the expression of MIR100HG and CALD1 was up-regulated, and the expression of miR-142-5p was down-regulated. Moreover, MIR100HG expression was positively correlated with the tumor grade and clinical grade of patients with bladder cancer. Overexpression of MIR100HG effectively promoted the proliferation, migration and invasion of 5,637 cells, inhibited the expression of miR-142-5p, and induced the expression of CALD1 in 5,637 cells. In addition, miR-142-5p inhibited CALD1 expression in bladder cancer cells through a direct association, and reversed the proliferation and CALD1 expression in 5,637 cells overexpressing of MIR100HG.Conclusion: MIR100HG regulates CALD1 expression by targeting miR-142-5p to inhibit the proliferation, migration and invasion of bladder cancer cells. MIR100HG is an independent prognostic factor for bladder cancer, with potential as a biomarker for the diagnosis and treatment of bladder cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

MIR100HG Regulates CALD1 Gene Expression by Targeting miR-142-5p to Affect the Progression of Bladder Cancer Cells in vitro, as Revealed by Transcriptome Sequencing

Zhang

Wang

et al. 2022

Front. Mol. Biosci.

View full text Add to dashboard Cite

show abstract

“…Caldesmon 1 (CALD1) [ 93 ] modulates actin filaments of the cytoskeleton, controlling cell morphology and movement. CALD1 expression is augmented in both neoplastic and vascular cells, and it confers worse clinical outcomes.…”

Section: Signaling Pathways Involved In Neovascularizationmentioning

confidence: 99%

The Vascular Microenvironment in Glioblastoma: A Comprehensive Review

Mosteiro

Pedrosa²,

Ferrés³

et al. 2022

Biomedicines

View full text Add to dashboard Cite

Glioblastoma multiforme, the deadliest primary brain tumor, is characterized by an excessive and aberrant neovascularization. The initial expectations raised by anti-angiogenic drugs were soon tempered due to their limited efficacy in improving the overall survival. Intrinsic resistance and escape mechanisms against anti-VEGF therapies evidenced that tumor angiogenesis is an intricate multifaceted phenomenon and that vessels not only support the tumor but exert indispensable interactions for resistance and spreading. This holistic review covers the essentials of the vascular microenvironment of glioblastoma, including the perivascular niche components, the vascular generation patterns and the implicated signaling pathways, the endothelial–tumor interrelation, and the interconnection between vessel aberrancies and immune disarrangement. The revised concepts provide novel insights into the preclinical models and the potential explanations for the failure of conventional anti-angiogenic therapies, leading to an era of new and combined anti-angiogenic-based approaches.

show abstract

“…A recent study of the mechanisms underlying the effect of l-CaD on microvascular facilitation and architecture in glioma showed that l-CaD is associated with abnormal microvessels in anaplastic astrocytoma and glioblastoma (an aggressive grade IV astrocytoma)[ 60 ]. The mechanism of such action was suggested by biofunction prediction to occur by modulating tumor angiogenesis, as ECs and pericytes were more apparent in the tumor microenvironment of high CALD1 expression samples.…”

Section: Cad Contributes To Tumor Angiogenesismentioning

confidence: 99%

“…The mechanism of such action was suggested by biofunction prediction to occur by modulating tumor angiogenesis, as ECs and pericytes were more apparent in the tumor microenvironment of high CALD1 expression samples. Histological and immunofluorescence examination of tumor tissue showed that CaD was associated with vessel architecture in astrocytoma and glioblastoma[ 60 - 63 ]. In stage III/IV mismatch-proficient CRC, CALD1 was upregulated and associated with angiogenesis, as detected by bioinformatics ‘Weighted gene coexpression network analysis’ (WGCNA)[ 41 ].…”

Section: Cad Contributes To Tumor Angiogenesismentioning

confidence: 99%

“…CALD1 expression was associated with a high pathological grade and poor clinical outcome in a bioinformatics analysis of glioma samples from the TCGA and Chinese Glioma Genome Atlas databases. “Biofunction prediction” suggested that CALD1 modulated tumor angiogenesis in these tumors[ 60 ]. Single-cell RNA sequencing (scRNA-seq), a technique that can define cellular states within both normal and disease tissues, including the immune phenotypes in the tumor microenvironment[ 114 ], showed that CALD1 was upregulated in neoplastic cells and was involved in the tumorigenic processes of gliomas.…”

Section: Role Of Cad In Other Cancer Typesmentioning

confidence: 99%

See 1 more Smart Citation

Emerging role of caldesmon in cancer: A potential biomarker for colorectal cancer and other cancers

Alnuaimi¹,

Nair²,

Malhab³

et al. 2022

WJGO

View full text Add to dashboard Cite

Colorectal cancer (CRC) is a devastating disease, mainly because of metastasis. As a result, there is a need to better understand the molecular basis of invasion and metastasis and to identify new biomarkers and therapeutic targets to aid in managing these tumors. The actin cytoskeleton and actin-binding proteins are known to play an important role in the process of cancer metastasis because they control and execute essential steps in cell motility and contractility as well as cell division. Caldesmon (CaD) is an actin-binding protein encoded by the CALD1 gene as multiple transcripts that mainly encode two protein isoforms: High-molecular-weight CaD, expressed in smooth muscle, and low-molecular weight CaD (l-CaD), expressed in nonsmooth muscle cells. According to our comprehensive review of the literature, CaD, particularly l-CaD, plays a key role in the development, metastasis, and resistance to chemoradiotherapy in colorectal, breast, and urinary bladder cancers and gliomas, among other malignancies. CaD is involved in many aspects of the carcinogenic hallmarks, including epithelial mesenchymal transition via transforming growth factor-beta signaling, angiogenesis, resistance to hormonal therapy, and immune evasion. Recent data show that CaD is expressed in tumor cells as well as in stromal cells, such as cancer-associated fibroblasts, where it modulates the tumor microenvironment to favor the tumor. Interestingly, CaD undergoes selective tumor-specific splicing, and the resulting isoforms are generally not expressed in normal tissues, making these transcripts ideal targets for drug design. In this review, we will analyze these features of CaD with a focus on CRC and show how the currently available data qualify CaD as a potential candidate for targeted therapy in addition to its role in the diagnosis and prognosis of cancer.

show abstract

CALD1 Modulates Gliomas Progression via Facilitating Tumor Angiogenesis

Cited by 18 publications

References 26 publications

MIR100HG Regulates CALD1 Gene Expression by Targeting miR-142-5p to Affect the Progression of Bladder Cancer Cells in vitro, as Revealed by Transcriptome Sequencing

MIR100HG Regulates CALD1 Gene Expression by Targeting miR-142-5p to Affect the Progression of Bladder Cancer Cells in vitro, as Revealed by Transcriptome Sequencing

The Vascular Microenvironment in Glioblastoma: A Comprehensive Review

Emerging role of caldesmon in cancer: A potential biomarker for colorectal cancer and other cancers

Contact Info

Product

Resources

About