scholarly journals Minimal dosing of leukocyte targeting TRAIL decreases triple-negative breast cancer metastasis following tumor resection

2019 ◽  
Vol 5 (7) ◽  
pp. eaaw4197 ◽  
Author(s):  
Nidhi Jyotsana ◽  
Zhenjiang Zhang ◽  
Lauren E. Himmel ◽  
Fang Yu ◽  
Michael R. King
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Primary Tumor ◽  
Cancer Metastasis ◽  
Triple Negative ◽  
Tumor Resection ◽  
Breast Cancer Metastasis ◽  
Surgical Removal ◽  
Secondary Tumors ◽  
Tumor Types

Surgical removal of the primary tumor is a common practice in breast cancer treatment. However, postsurgical metastasis poses an immense setback in cancer therapy. Considering that 90% of cancer-related deaths are due to metastasis, antimetastatic therapeutic strategies that can target disseminating tumor cells in the circulation before they can form secondary tumors hold preclinical and clinical potential for cancer patients. Our current work uses a liposomal formulation functionalized with the adhesion receptor E-selectin and the apoptosis-inducing ligand TNF (tumor necrosis factor)–related apoptosis-inducing ligand (TRAIL) to reduce metastasis following tumor resection in an aggressive triple-negative breast cancer (TNBC) mouse model. We demonstrate that minimal administration of E-selectin–TRAIL liposomes can target metastasis in a TNBC model, with primary tumor resection to mimic clinical settings. Our study indicates that TRAIL liposomes, alone or in combination with existing clinically approved therapies, may neutralize distant metastasis of a broad range of tumor types systemically.

scholarly journals CPSF4 promotes triple negative breast cancer metastasis by upregulating MDM4

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Kaping Lee ◽  
Qiufan Zheng ◽  
Qianyi Lu ◽  
Fei Xu ◽  
Ge Qin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Cancer Metastasis ◽  
Triple Negative ◽  
Breast Cancer Metastasis

scholarly journals DCAF13 promotes triple-negative breast cancer metastasis by mediating DTX3 mRNA degradation

Cell Cycle ◽  
2020 ◽  
Vol 19 (24) ◽  
pp. 3622-3631
Author(s):  
Jiazhe Liu ◽  
Hongchang Li ◽  
Anwei Mao ◽  
Jingfeng Lu ◽  
Weiyan Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Cancer Metastasis ◽  
Triple Negative ◽  
Mrna Degradation ◽  
Breast Cancer Metastasis

scholarly journals MicroRNA-200b targets protein kinase Cα and suppresses triple-negative breast cancer metastasis

2014 ◽  
Vol 35 (10) ◽  
pp. 2254-2263 ◽  
Author(s):  
Brock Humphries ◽  
Zhishan Wang ◽  
Aaron L. Oom ◽  
Theresa Fisher ◽  
Dongfeng Tan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Kinase ◽  
Triple Negative Breast Cancer ◽  
Cancer Metastasis ◽  
Triple Negative ◽  
Breast Cancer Metastasis ◽  
Protein Kinase Cα

scholarly journals Sanguisorba officinalis L. Suppresses Triple-Negative Breast Cancer Metastasis by Inhibiting Late-Phase Autophagy via Hif-1α/Caveolin-1 Signaling

2020 ◽  
Vol 11 ◽  
Author(s):  
Neng Wang ◽  
Gulizeba Muhetaer ◽  
Xiaotong Zhang ◽  
Bowen Yang ◽  
Caiwei Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Molecular Mechanisms ◽  
Cancer Metastasis ◽  
Triple Negative ◽  
Late Phase ◽  
Breast Cancer Metastasis ◽  
Chinese Herbs ◽  
Caveolin 1 ◽  
Sanguisorba Officinalis

Sanguisorba officinalis L. (SA) is a common herb for cancer treatment in the clinic, particularly during the consolidation phase to prevent occurrence or metastasis. Nevertheless, there are limited studies reporting the molecular mechanisms about its anti-metastatic function. It is well demonstrated that autophagy is one of the critical mechanisms accounting for metastasis and anti-cancer pharmacological actions of Chinese herbs. On the threshold, the regulatory effects and molecular mechanisms of SA in suppressing autophagy-related breast cancer metastasis were investigated in this study. In vitro findings demonstrated that SA potently suppressed the proliferation, colony formations well as metastasis process in triple-negative breast cancer. Network and biological analyses predicted that SA mainly targeted caveolin-1 (Cav-1) to induce anti-metastatic effects, and one of the core mechanisms was via regulation of autophagy. Further experiments—including western blotting, transmission electron microscopy, GFP-mRFP-LC3 immunofluorescence, and lysosomal-activity detection—validated SA as a potent late-stage autophagic inhibitor by increasing microtubule-associated light chain 3-II (LC3-II) conversion, decreasing acidic vesicular-organelle formation, and inducing lysosomal dysfunction even under conditions of either starvation or hypoxia. Furthermore, the anti-autophagic and anti-metastatic activity of SA was Cav-1-dependent. Specifically, Cav-1 knockdown significantly facilitated SA-mediated inhibition of autophagy and metastasis. Furthermore, hypoxia inducible factor-1α (Hif-1α) overexpression attenuated the SA-induced inhibitory activities on Cav-1, autophagy, and metastasis, indicating that SA may have inhibited autophagy-related metastasis via Hif-1α/Cav-1 signaling. In both mouse breast cancer xenograft and zebrafish xenotransplantation models, SA inhibited breast cancer growth and inhibited late-phase autophagy in vivo, which was accompanied by suppression of Hif-1α/Cav-1 signaling and the epithelial-mesenchymal transition. Overall, our findings not only indicate that SA acts as a novel late-phase autophagic inhibitor with anti-metastatic activities in triple-negative breast cancer, but also highlight Cav-1 as a regulator in controlling late-phase autophagic activity.

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