RhoBTB3 Regulates Proliferation and Invasion of Breast Cancer Cells via Col1a1

Kim, Kyungho; Kim, Youn‐Jae

doi:10.14348/molcells.2022.2037

Cited by 14 publications

(7 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…While overall breast cancer survival has steadily increased, with a reported rate of 91% by 2020 ( Kim and Kim, 2022 ; Viale, 2020 ), TNBC, the most aggressive and difficult-to-treat subtype, has a 5-year survival rate of 77% ( Giaquinto et al, 2022 ). Hormone therapy and HER2 targeting are ineffective for TNBC and chemotherapy is the main treatment modality, particularly at the metastatic stage ( Wahba and El-Hadaad, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Microtubule Acetylation-Specific Inhibitors Induce Cell Death and Mitotic Arrest via JNK/AP-1 Activation in Triple-Negative Breast Cancer Cells

Ahn

Kwon

et al. 2023

Molecules and Cells

View full text Add to dashboard Cite

Microtubule acetylation has been proposed as a marker of highly heterogeneous and aggressive triple-negative breast cancer (TNBC). The novel microtubule acetylation inhibitors GM-90257 and GM-90631 (GM compounds) cause TNBC cancer cell death but the underlying mechanisms are currently unknown. In this study, we demonstrated that GM compounds function as anti-TNBC agents through activation of the JNK/AP-1 pathway. RNA-seq and biochemical analyses of GM compound-treated cells revealed that c-Jun N-terminal kinase (JNK) and members of its downstream signaling pathway are potential targets for GM compounds. Mechanistically, JNK activation by GM compounds induced an increase in c-Jun phosphorylation and c-Fos protein levels, thereby activating the activator protein-1 (AP-1) transcription factor. Notably, direct suppression of JNK with a pharmacological inhibitor alleviated Bcl2 reduction and cell death caused by GM compounds. TNBC cell death and mitotic arrest were induced by GM compounds through AP-1 activation in vitro. These results were reproduced in vivo, validating the significance of microtubule acetylation/ JNK/AP-1 axis activation in the anti-cancer activity of GM compounds. Moreover, GM compounds significantly attenuated tumor growth, metastasis, and cancer-related death in mice, demonstrating strong potential as therapeutic agents for TNBC.

show abstract

Section: Discussionmentioning

confidence: 99%

Microtubule Acetylation-Specific Inhibitors Induce Cell Death and Mitotic Arrest via JNK/AP-1 Activation in Triple-Negative Breast Cancer Cells

Ahn

Kwon

et al. 2023

Molecules and Cells

View full text Add to dashboard Cite

show abstract

“…1 ). 7 21 This process functions as a safeguard, inhibiting the attachment of aberrant cells at inappropriate locations or the proliferation of dysplastic cells. Upon detachment, death receptors and mitochondria-mediated apoptotic pathways trigger anoikis.…”

Section: Anchorage Independence In Cancer Metastasismentioning

confidence: 99%

Anchorage Dependence and Cancer Metastasis

Lee,

Oh,

Park

et al. 2024

J Korean Med Sci

View full text Add to dashboard Cite

The process of cancer metastasis is dependent on the cancer cells’ capacity to detach from the primary tumor, endure in a suspended state, and establish colonies in other locations. Anchorage dependence, which refers to the cells’ reliance on attachment to the extracellular matrix (ECM), is a critical determinant of cellular shape, dynamics, behavior, and, ultimately, cell fate in nonmalignant and cancer cells. Anchorage-independent growth is a characteristic feature of cells resistant to anoikis, a programmed cell death process triggered by detachment from the ECM. This ability to grow and survive without attachment to a substrate is a crucial stage in the progression of metastasis. The recently discovered phenomenon named “adherent-to-suspension transition (AST)” alters the requirement for anchoring and enhances survival in a suspended state. AST is controlled by four transcription factors (IKAROS family zinc finger 1, nuclear factor erythroid 2, BTG anti-proliferation factor 2, and interferon regulatory factor 8) and can detach cells without undergoing the typical epithelial-mesenchymal transition. Notably, AST factors are highly expressed in circulating tumor cells compared to their attached counterparts, indicating their crucial role in the spread of cancer. Crucially, the suppression of AST substantially reduces metastasis while sparing primary tumors. These findings open up possibilities for developing targeted therapies that inhibit metastasis and emphasize the importance of AST, leading to a fundamental change in our comprehension of how cancer spreads.

show abstract

“… 35 Furthermore, RhoBTB3 can regulate breast cancer progression by controlling collagen deposition, specifically, knockdown of RhoBTB3 regulates breast cancer cell proliferation and invasion, accompanied by the reduction of COL1A1. 36 MRTF-A physically interacts with the promoter of COL1A1 to facilitate the acetylation of chromatin and the recruitment of RNA polymerase II in breast cancer. 37 In addition, COL1A1 is associated with immune and tumor microenvironment.…”

Section: Collagen Type I Alpha 1 Chain (Col1a1)mentioning

confidence: 99%

Unveiling Collagen’s Role in Breast Cancer: Insights into Expression Patterns, Functions and Clinical Implications

Li,

Jin,

Xue

2024

IJGM

View full text Add to dashboard Cite

Collagen, the predominant protein constituent of the mammalian extracellular matrix (ECM), comprises a diverse family of 28 members (I–XXVIII). Beyond its structural significance, collagen is implicated in various diseases or cancers, notably breast cancer, where it influences crucial cellular processes including proliferation, metastasis, apoptosis, and drug resistance, intricately shaping cancer progression and prognosis. In breast cancer, distinct collagens exhibit differential expression profiles, with some showing heightened or diminished levels in cancerous tissues or cells compared to normal counterparts, suggesting specific and pivotal biological functions. In this review, we meticulously analyze the expression of individual collagen members in breast cancer, utilizing Transcripts Per Million (TPM) data sourced from the GEPIA2 database. Through this analysis, we identify collagens that deviate from normal expression patterns in breast cancer, providing a comprehensive overview of their expression dynamics, functional roles, and underlying mechanisms. Our findings shed light on recent advancements in understanding the intricate interplay between these aberrantly expressed collagens and breast cancer. This exploration aims to offer valuable insights for the identification of potential biomarkers and therapeutic targets, thereby advancing the prospects of more effective interventions in breast cancer treatment.

show abstract

RhoBTB3 Regulates Proliferation and Invasion of Breast Cancer Cells via Col1a1

Cited by 14 publications

References 57 publications

Microtubule Acetylation-Specific Inhibitors Induce Cell Death and Mitotic Arrest via JNK/AP-1 Activation in Triple-Negative Breast Cancer Cells

Microtubule Acetylation-Specific Inhibitors Induce Cell Death and Mitotic Arrest via JNK/AP-1 Activation in Triple-Negative Breast Cancer Cells

Anchorage Dependence and Cancer Metastasis

Unveiling Collagen’s Role in Breast Cancer: Insights into Expression Patterns, Functions and Clinical Implications

Contact Info

Product

Resources

About