<i>ARID1A</i> knockdown enhances carcinogenesis features and aggressiveness of Caco-2 colon cancer cells: An <i>in vitro</i> cellular mechanism study

Peerapen, Paleerath; Sueksakit, Kanyarat; Boonmark, Wanida; Yoodee, Sunisa; Thongboonkerd, Visith

doi:10.7150/jca.65511

Cited by 11 publications

(11 citation statements)

References 79 publications

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“…Ovarian cancer, melanoma and stomach cancer Fu et al [227], Li et al [228], Peerpen et al [229], and Zhao et al [230] PLK4-kinase overexpressed in PGCCs, and descendant cells showed strong migration and invasion abilities. Its interaction with CDC25C is associated with the formation of PGCCs.…”

Section: Liu Et Al [218] Andmentioning

confidence: 99%

Biomarkers in Breast Cancer: An Old Story with a New End

Alves

Meira

Merigueti

et al. 2023

Genes

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Breast cancer is the second most frequent cancer in the world. It is a heterogeneous disease and the leading cause of cancer mortality in women. Advances in molecular technologies allowed for the identification of new and more specifics biomarkers for breast cancer diagnosis, prognosis, and risk prediction, enabling personalized treatments, improving therapy, and preventing overtreatment, undertreatment, and incorrect treatment. Several breast cancer biomarkers have been identified and, along with traditional biomarkers, they can assist physicians throughout treatment plan and increase therapy success. Despite the need of more data to improve specificity and determine the real clinical utility of some biomarkers, others are already established and can be used as a guide to make treatment decisions. In this review, we summarize the available traditional, novel, and potential biomarkers while also including gene expression profiles, breast cancer single-cell and polyploid giant cancer cells. We hope to help physicians understand tumor specific characteristics and support decision-making in patient-personalized clinical management, consequently improving treatment outcome.

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Section: Liu Et Al [218] Andmentioning

confidence: 99%

Biomarkers in Breast Cancer: An Old Story with a New End

Alves

Meira

Merigueti

et al. 2023

Genes

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“…Western blot analyses for ARID1A, β-actin and GAPDH (loading control) were performed as described previously [ 21 , 22 ]. Details are also provided in Additional file 2 .…”

Section: Methodsmentioning

confidence: 99%

“…To address functional roles of ARID1A and its selected interactor, β-actin, siRNA transfection was performed for single and double gene knockdowns in MDCK renal cells. Details of siRNA transfection have been described previously [ 21 , 22 ] and are also provided in Additional file 2 .…”

Section: Methodsmentioning

confidence: 99%

“…Similarly, knockdown of ARID1A in human ECs activates secretion of ANG2 and promotes ECs proliferation, migration and formation of capillary/mesh-like tubes [ 19 ]. Besides, the increase of vascular endothelial growth factor (VEGF), another essential angiogenic factor, has been found in the ARID1A -deficient breast [ 20 ] and colon [ 21 ] cancer cells.…”

Section: Introductionmentioning

confidence: 99%

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Identification and characterization of ARID1A-interacting proteins in renal tubular cells and their molecular regulation of angiogenesis

Yoodee,

Peerapen,

Plumworasawat

et al. 2023

J Transl Med

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Background Defects and deficiency of AT-rich interactive domain-containing protein 1A (ARID1A) encoded by a tumor suppressor gene ARID1A have recently been suggested to get involved in angiogenesis, a crucial process in carcinogenesis. However, molecular mechanisms of ARID1A deficiency to induce angiogenesis in kidney cancer remain underinvestigated. Methods We performed large-scale identification of ARID1A protein interactors in renal tubular epithelial cells (RTECs) using immunoprecipitation (IP) followed by nanoLC-ESI-LTQ-Orbitrap tandem mass spectrometry (MS/MS). Their roles in angiogenesis were investigated using various assays. Results A total of 74 ARID1A-interacting proteins were identified. Protein–protein interactions analysis revealed that these identified proteins interacted directly or indirectly with ARID1A. Among them, the direct interaction between ARID1A and β-actin was validated by IP and reciprocal IP followed by Western blotting. Small interfering RNA (siRNA) was used for single and double knockdowns of ARID1A and ACTB. Semi-quantitative RT-PCR demonstrated that deficiency of ARID1A, but not ACTB, significantly affected expression of angiogenesis-related genes in RTECs (VEGF and FGF2 were increased, whereas PDGF and EGF were decreased). However, the knockdowns did not affect TGFB1 and FGF1 levels. The quantitative mRNA expression data of VEGF and TGFB1 were consistent with the secreted levels of their protein products as measured by ELISA. Only secreted products derived from ARID1A-deficient RTECs significantly increased endothelial cells (ECs) migration and tube formation. Some of the other carcinogenic features could also be confirmed in the ARID1A-deficient RTECs, including increased cell migration and chemoresistance. Double knockdowns of both ARID1A and ACTB did not enhance the effects of single ARID1A knockdown in all assays. Conclusions We report herein a large dataset of the ARID1A-interacting proteins in RTECs using an IP-MS/MS approach and confirm the direct interaction between ARID1A and β-actin. However, the role of ARID1A deficiency in angiogenesis is independent of β-actin.

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“…AT-Rich Interactive Domain-containing protein 1A (ARID1A), as one of the components making up the largest SWI/SNF subunit together with AT-Rich Interactive Domain-containing protein 1B (ARID1B), is the most frequent target of SWI/SNF mutations. mutations in ARID1A impair enhancer-mediated gene regulation and prognosis in patients with colon cancer ( 124 , 125 ). Interestingly, SWI/SNF complex stability is also vital for tumor cell viability, which might be impaired by ARID1A mutation.…”

Section: Mechanisms Of Immunotherapy Resistancementioning

confidence: 99%

Mechanism and strategies of immunotherapy resistance in colorectal cancer

et al. 2022

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Colorectal cancer (CRC) is the third most common cancer in the world. Although there are standard treatment options for CRC, most patients respond poorly to these treatments. Immunotherapies have gradually emerged due to the increasing awareness and understanding of tumor immunity, exhibiting good therapeutic efficacy in various cancers. Immunotherapies include cytokines, immune checkpoint inhibitors (ICIs), and adoptive cell therapies. In particular, ICIs, which are antibodies against cytotoxic T lymphocyte-associated protein 4 (CTLA-4), programmed cell death 1 (PD-1), or its ligand PD-L1, have been successfully applied clinically for solid tumors, relieving the inhibitory effect of the tumor microenvironment on T cells. However, only a minority of patients with cancer achieve a durable clinical response during immunotherapy. Several factors restrict the efficacy of immunotherapy, leading to the development of drug resistance. In this review, we aimed to discuss the current status of immunotherapy for CRC and elaborate on the mechanisms that mediate resistance to immunotherapy and other potential therapeutic strategies.

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ARID1A knockdown enhances carcinogenesis features and aggressiveness of Caco-2 colon cancer cells: An in vitro cellular mechanism study

Cited by 11 publications

References 79 publications

Biomarkers in Breast Cancer: An Old Story with a New End

Biomarkers in Breast Cancer: An Old Story with a New End

Identification and characterization of ARID1A-interacting proteins in renal tubular cells and their molecular regulation of angiogenesis

Mechanism and strategies of immunotherapy resistance in colorectal cancer

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