Progress in immune checkpoint inhibition in early-stage triple-negative breast cancer

Mohamed, Ahmed; Kruse, Megan; Tran, Jennifer

doi:10.1080/14737140.2023.2262764

Cited by 2 publications

(2 citation statements)

References 77 publications

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“…At present, there are many treatments for breast cancer including surgery, radiotherapy, chemotherapy, estrogen receptor modulators, estrogen receptor antagonists, sulfatase inhibitors, immune checkpoint inhibitors, and so on ( 53 - 58 ). Task of treating breast cancer remains daunting.…”

Section: Discussionmentioning

confidence: 99%

Sinensetin suppresses breast cancer cell progression via Wnt/β-catenin pathway inhibition

Zhu,

Meng,

Wei

et al. 2024

Transl Cancer Res

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Background Although there are many treatments for breast cancer, such as surgery, radiotherapy, chemotherapy, estrogen receptor antagonists, immune checkpoint inhibitors and so on. However, safer and more effective therapeutic drugs for breast cancer are needed. Sinensetin, a safer therapeutic drugs, come from citrus species and medicinal plants used in traditional medicine, while its role and underlying mechanism in breast cancer remain unclear. Our study aimed to investigate the role and mechanism of sinensetin in breast cancer. Methods Cell Counting Kit-8 (CCK-8) was used to determine the safe concentration of sinensetin in MCF-10A, MCF7 and MDA-MB-231 cells; 120 μM sinensetin was used in subsequent experiments. Real time polymerase chain reaction (RT-PCR), Western blotting, Terminal Deoxynucleotidyl Transferase mediated dUTP Nick-End Labeling (TUNEL) apoptosis assay, Transwell invasion assay and Clone formation assay were used in this study to determine cell viability, mRNA expression, protein levels, apoptosis, proliferation, invasion and so on. Results Herein, our results showed that 120 μM sinensetin suppressed the cell viability and promoted apoptosis of MCF7 and MDA-MB-231 cells. Treatment with 120 µM sinensetin for 24 h showed no significant toxicity to normal mammary cells; 120 μM sinensetin decreased cell proliferation, invasion, and epithelial-mesenchymal transition (EMT), and downregulated β-catenin, lymphatic enhancing factor 1 (LEF1), T-cell factor (TCF) 1/TCF7, and TCF3/TCF7L1 expression in MCF7 and MDA-MB-231 cells. The Wnt agonist SKL2001 reversed the inhibitory effect of sinensetin on cell survival, metastasis, and EMT. Sinensetin-induced downregulation of β-catenin, LEF1, and TCF1/TCF7 expression were upregulated by SKL2001 in MCF7 and MDA-MB-231 cells. Conclusions In summary, sinensetin suppressed the metastasis of breast cancer cell via inhibition of Wnt/β-catenin pathway and there were no adverse effects on normal breast cells. Our study confirmed the role of sinensetin in breast cancer cells and provided a better understanding of the underlying mechanism.

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Section: Discussionmentioning

confidence: 99%

Sinensetin suppresses breast cancer cell progression via Wnt/β-catenin pathway inhibition

Zhu,

Meng,

Wei

et al. 2024

Transl Cancer Res

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“…Additionally, atezolizumab, durvalumab, and CTLA-4 inhibitors are being studied as possible therapeutic agents. However, these studies are still ongoing [71].…”

Section: Tumor Immune Microenvironmentmentioning

confidence: 99%

Translational Aspects in Metaplastic Breast Carcinoma

Barrientos-Toro,

Ding,

Raso

2024

Cancers

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Breast cancer is the most common cancer among women. Metaplastic breast carcinoma (MpBC) is a rare, heterogeneous group of invasive breast carcinomas, which are classified as predominantly triple-negative breast carcinomas (TNBCs; HR-negative/HER2-negative). Histologically, MpBC is classified into six subtypes. Two of these are considered low-grade and the others are high-grade. MpBCs seem to be more aggressive, less responsive to neoadjuvant chemotherapy, and have higher rates of chemoresistance than other TNBCs. MpBCs have a lower survival rate than expected for TNBCs. MpBC treatment represents a challenge, leading to a thorough exploration of the tumor immune microenvironment, which has recently opened the possibility of new therapeutic strategies. The epithelial–mesenchymal transition in MpBC is characterized by the loss of intercellular adhesion, downregulation of epithelial markers, underexpression of genes with biological epithelial functions, upregulation of mesenchymal markers, overexpression of genes with biological mesenchymal functions, acquisition of fibroblast-like (spindle) morphology, cytoskeleton reorganization, increased motility, invasiveness, and metastatic capabilities. This article reviews and summarizes the current knowledge and translational aspects of MpBC.

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Progress in immune checkpoint inhibition in early-stage triple-negative breast cancer

Cited by 2 publications

References 77 publications

Sinensetin suppresses breast cancer cell progression via Wnt/β-catenin pathway inhibition

Sinensetin suppresses breast cancer cell progression via Wnt/β-catenin pathway inhibition

Translational Aspects in Metaplastic Breast Carcinoma

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