Characteristics, behaviour and role of biomarkers in metastatic triple-negative breast cancer

Goto, Y; Thike, Aye Aye; Ong, Clara Chong Hui; Lim, Jimmy; Nasir, Nur Diyana Md; Li, Huihua; Koh, Valerie Cui Yun; Chen, Xiao Yang; Yeong, Joe Poh Sheng; Sasano, Hironobu; Tan, Puay Hoon

doi:10.1136/jclinpath-2019-206078

Cited by 8 publications

(4 citation statements)

References 59 publications

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“…2 At present, the 5-year survival rate of TNBC is less than 30%. 3 In recent years transcriptional profiling has been used to classify breast cancers into at least five molecular subtypes (basal, claudin-low, luminal A, luminal B, and HER2-enriched). 4 TNBC was mainly composed of basal-like breast cancer (BLBC, 39-54%) and CLBC (25-39%).…”

Section: Introductionmentioning

confidence: 99%

<p>Targeting PIK3CG in Combination with Paclitaxel as a Potential Therapeutic Regimen in Claudin-Low Breast Cancer</p>

Chang¹,

Ling²,

Liu³

et al. 2020

CMAR

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Purpose: Molecular targeting is a powerful approach for aggressive claudin-low breast cancer (CLBC). Overexpression of PI3K catalytic subunit gamma (PIK3CG) in human CLBC is offering a promising opportunity for targeted therapies. We utilized a specific inhibitor of PIK3CG combined with paclitaxel (PTX) to treat CLBC cells in vitro and in vivo. Patients and Methods: The tumor cells growth and apoptosis in vitro were analyzed by CCK8, plate clone formation assay, tumorsphere assay, Hoechst staining and flow cytometry. The invasion and metastasis ability of tumor cells in vitro were investigated by wound healing and transwell experiments. Critical gene expression levels were checked by qRT-PCR and Western blot. Xenograft models with CLBC cell lines in SCID mice were established to investigate the effect of combined drugs in vivo. Results: We identified that PIK3CG was a potential therapeutic target for CLBC patients. Targeting PIK3CG potentiated CLBC cells growth inhibition in 2D and 3D cultures by PTX. Inhibition of PIK3CG activation could enhance CLBC cells apoptosis and migration suppression induced by PTX. Manipulating autophagy was a validated approach for the use of PIK3CG inhibitor. Using CLBC xenograft mice model, we found that CLBC tumors in vivo could be well treated by combined drugs of PIK3CG inhibitor and PTX. Conclusion: We demonstrated that PIK3CG was a potential target for the therapy of CLBC and inhibition of PIK3CG activation could reinforce the therapeutic effect of this aggressive disease by PTX. The combined use of PIK3CG inhibitor and PTX might be a potential regimen for treating this subtype of breast cancer.

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Section: Introductionmentioning

confidence: 99%

<p>Targeting PIK3CG in Combination with Paclitaxel as a Potential Therapeutic Regimen in Claudin-Low Breast Cancer</p>

Chang¹,

Ling²,

Liu³

et al. 2020

CMAR

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“…Its gene product “p53” protein showed 90% missense mutation from CpG sites that span 190 diverse codons in the TP53 gene exon that code the DNA-binding region of the p53 protein [ 68 ]. As a result, p53 losses its function, no or poor DNA binding, and restricted transcription [ 69 , 72 , 73 ] caused enhancement in tumour-infiltrating lymphocytes in the stroma [ 73 ], epithelial-mesenchymal transition, high rate of tumorigenesis, cellular invasion/migration, drug resistance, rapid cell division in TNBC cell lines [ 74 , 75 ], and large-sized tumour growth in females [ 76 ]. Similarly, the R330 frame-shift mutation in the coding region at the C-terminus of the GATA3 gene leads to variations in epithelial to mesenchymal tissues causing overexpression and abnormal regulation of breast cell growth and progression.…”

Section: Triple-negative Breast Cancermentioning

confidence: 99%

Nanomaterial-assisted CRISPR gene-engineering – A hallmark for triple-negative breast cancer therapeutics advancement

Farheen¹,

Hosmane²,

Zhao³

et al. 2022

Materials Today Bio

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“…Despite the controversy regarding the correlation between the expression of AR and ER-β in TNBC, it is important to remember that ER-β is co-expressed with AR and may play a suppressive role in a subset of TNBC such as LAR tumors or apocrine carcinomas, suggesting the need for their combined consideration in the treatment of these tumors. Goto et al examined the combined expression of AR, ER-β, and P53 in metastatic TNBC, and showed that AR-/ER-β+/P53+ was significantly correlated with a poorer outcome [ 113 ].…”

Section: The Role Of Each Sex Steroid Hormone In Tnbc In a Clinical Settingmentioning

confidence: 99%

Carcinogenesis of Triple-Negative Breast Cancer and Sex Steroid Hormones

Honma

Matsuda

Mikami

2021

Cancers

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Triple-negative breast cancer (TNBC) lacks an effective treatment target and is usually associated with a poor clinical outcome; however, hormone unresponsiveness, which is the most important biological characteristic of TNBC, only means the lack of nuclear estrogenic signaling through the classical estrogen receptor (ER), ER-α. Several sex steroid receptors other than ER-α: androgen receptor (AR), second ER, ER-β, and non-nuclear receptors represented by G-protein-coupled estrogen receptor (GPER), are frequently expressed in TNBC and their biological and clinical importance has been suggested by a large number of studies. Despite the structural similarity between each sex steroid hormone (androgens and estrogens) or each receptor (AR and ER-β), and similarity in the signaling mechanisms of these hormones, most studies or reviews focused on one of these receptors, and rarely reviewed them in a comprehensive way. Considering the coexistence of these hormones and their receptors in TNBC in a clinical setting, a comprehensive viewpoint would be important to correctly understand the association between the carcinogenic mechanism or pathobiology of TNBC and sex steroid hormones. In this review, the carcinogenic or pathobiological role of sex steroid hormones in TNBC is considered, focusing on the common and divergent features of the action of these hormones.

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Characteristics, behaviour and role of biomarkers in metastatic triple-negative breast cancer

Cited by 8 publications

References 59 publications

<p>Targeting PIK3CG in Combination with Paclitaxel as a Potential Therapeutic Regimen in Claudin-Low Breast Cancer</p>

<p>Targeting PIK3CG in Combination with Paclitaxel as a Potential Therapeutic Regimen in Claudin-Low Breast Cancer</p>

Nanomaterial-assisted CRISPR gene-engineering – A hallmark for triple-negative breast cancer therapeutics advancement

Carcinogenesis of Triple-Negative Breast Cancer and Sex Steroid Hormones

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