☆ 4.7 Meeting Abstract

Targeting the Hedgehog signalling pathway in triple negative breast cancer.

JOURNAL OF CLINICAL ONCOLOGY (2018)

Journal

JOURNAL OF CLINICAL ONCOLOGY

Volume 36, Issue 15, Pages -

Publisher

AMER SOC CLINICAL ONCOLOGY

DOI: 10.1200/JCO.2018.36.15_suppl.e24216

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Curcumin inhibits the invasion and metastasis of triple negative breast cancer via Hedgehog/Gli1 signaling pathway

Mengjie Li, Tingting Guo, Jiayi Lin, Xia Huang, Qiaodan Ke, Yujian Wu, Chunping Fang, Chenxia Hu

Summary: Curcumin, the main pharmacological component extracted from Curcuma longa L, has been found to inhibit proliferation and metastasis of TNBC cells via the Hedgehog/Gli1 pathway, providing potential therapeutic strategies for TNBC.

JOURNAL OF ETHNOPHARMACOLOGY (2022)

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Article Multidisciplinary Sciences

Targeting cuproptosis by zinc pyrithione in triple-negative breast cancer

Xu Yang, Li Deng, Xianhong Diao, Siyuan Yang, Li Zou, Qin Yang, Jian Li, Jianyun Nie, Lina Zhao, Baowei Jiao

Summary: The compound zinc pyrithione (ZnPT) has been identified as a potent inhibitor of triple-negative breast cancer (TNBC) progression by disrupting copper homeostasis, offering a potential experimental foundation for exploring cuproptosis as a target for drug discovery in TNBC patients.

ISCIENCE (2023)

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Article Medicine, General & Internal

Potassium channel-driven bioelectric signalling regulates metastasis in triple-negative breast cancer

Samantha L. Payne, Priyanka Ram, Deepti H. Srinivasan, Thanh T. Le, Michael Levin, Madeleine J. Oudin

Summary: This study reveals that altering the resting membrane potential (RMP) of triple-negative breast cancer cells through manipulating potassium channel expression increases invasion and metastasis, accompanied by changes in gene expression related to cell adhesion. The study also identifies a new strategy to target metastatic breast cancer by repurposing an FDA-approved potassium channel blocker. These findings demonstrate that bioelectricity regulates cancer cell invasion and metastasis, potentially leading to new therapeutics for patients with metastatic disease.

EBIOMEDICINE (2022)

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Review Biochemistry & Molecular Biology

Targeting Triple Negative Breast Cancer With Oncolytic Adenoviruses

Gabriela Green-Tripp, Callum Nattress, Gunnel Hallden

Summary: Breast cancer is the most common cancer globally, and triple-negative breast cancer has a poor prognosis and higher risk. Oncolytic adenoviruses may provide a new strategy for improving the treatment outcome of breast cancer. Preclinical studies and clinical trials have shown the potential therapeutic efficacy of oncolytic adenoviruses in breast cancer.

FRONTIERS IN MOLECULAR BIOSCIENCES (2022)

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Review Medicine, Research & Experimental

Ferroptosis induction via targeting metabolic alterations in triple-negative breast cancer

Yaru Wang, Yue Sun, Feiran Wang, Hongyi Wang, Jing Hu

Summary: This article reviews the connection between ferroptosis and amino acid, iron, and lipid metabolism in triple-negative breast cancer (TNBC), discussing the potential significance and application prospects of ferroptosis as a treatment approach.

BIOMEDICINE & PHARMACOTHERAPY (2023)

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Letter Medicine, General & Internal

Pembrolizumab in Triple-Negative Breast Cancer

Ryan Sun, Lee-Jen Wei

Summary: This article discusses the clinical benefits of pembrolizumab combined with chemotherapy in patients with triple-negative breast cancer. The authors suggest that both hazard values and ratios should be considered when evaluating clinical benefits.

NEW ENGLAND JOURNAL OF MEDICINE (2022)

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Review Biochemistry & Molecular Biology

Targeting Triple-Negative Breast Cancer by the Phytopolyphenol Carnosol: ROS-Dependent Mechanisms

Halima Alsamri, Yusra Al Dhaheri, Rabah Iratni

Summary: Triple-negative breast cancer (TNBC) lacks the expression of hormone receptors and is highly aggressive and lethal. Conventional therapies and chemotherapeutic agents have limited effectiveness against TNBC. Phytochemicals, such as carnosol, have shown efficacy against TNBC by targeting key pathways involved in cancer development and progression. This review discusses the molecular mechanisms of carnosol in inhibiting TNBC and identifies it as a potential novel targeting protein degradation molecule.

ANTIOXIDANTS (2023)

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Article Oncology

Sulforaphane suppresses metastasis of triple-negative breast cancer cells by targeting the RAF/MEK/ERK pathway

Ying Zhang, Qian Lu, Nan Li, Ming Xu, Tatsuo Miyamoto, Jing Liu

Summary: Sulforaphane (SFN), a natural compound derived from broccoli, has been found to significantly inhibit migration and invasion of breast cancer cells by affecting cytoskeleton formation. SFN can also directly bind to RAF family proteins and inhibit phosphorylation of the signaling pathway. These findings suggest that SFN has the potential to be used as a therapeutic drug to inhibit breast cancer cell metastasis.

NPJ BREAST CANCER (2022)

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Article Cell Biology

Melatonin inhibits triple-negative breast cancer progression through the Lnc049808-FUNDC1 pathway

Anli Yang, Fu Peng, Lewei Zhu, Xing Li, Shunling Ou, Zhongying Huang, Song Wu, Cheng Peng, Peng Liu, Yanan Kong

Summary: Melatonin treatment downregulated FUNDC1 and lnc049808 in TNBC cell lines, which inhibited cell proliferation, invasion, and metastasis. lnc049808 and FUNDC1 acted as competing endogenous RNAs binding to miR-101, indicating a potential therapeutic pathway for TNBC progression inhibition by melatonin.

CELL DEATH & DISEASE (2021)

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Article Chemistry, Medicinal

Discovery of precision targeting EZH2 degraders for triple-negative breast cancer

Cheng Wang, Xinye Chen, Xingchen Liu, Dehua Lu, Shang Li, Lailiang Qu, Fucheng Yin, Heng Luo, Yonglei Zhang, Zhongwen Luo, Ningjie Cui, Lingyi Kong, Xiaobing Wang

Summary: EZH2 is often overexpressed in TNBC and other tumors, affecting tumor development and prognosis. The designed PROTACs molecule U3i precision targets EZH2 and shows good inhibitory effects on TNBC cells, inducing apoptosis without causing much damage to normal cells. U3i is a potential anticancer molecule for TNBC treatment.

EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY (2022)

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Article Biochemistry & Molecular Biology

Targeting Cell Death Mechanism Specifically in Triple Negative Breast Cancer Cell Lines

Lavinia-Lorena Pruteanu, Cornelia Braicu, Dezso Modos, Maria-Ancuta Jurj, Lajos-Zsolt Raduly, Oana Zanoaga, Lorand Magdo, Roxana Cojocneanu, Sergiu Pasca, Cristian Moldovan, Alin Iulian Moldovan, Adrian Bogdan Tigu, Eugen Gurzau, Lorentz Jantschi, Andreas Bender, Ioana Berindan-Neagoe

Summary: This study evaluated the effect of arsenate on triple negative breast cancer (TNBC) cells and found that arsenate induced cytoskeletal alteration, autophagy, and apoptosis. TNBC cells showed a more prominent response to arsenate compared to other cell lines.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2022)

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Article Multidisciplinary Sciences

EBF1 promotes triple-negative breast cancer progression by surveillance of the HIF1α pathway

Zhaoping Qiu, Weijie Guo, Bo Dong, Yu Wang, Pan Deng, Chi Wang, Jinpeng Liu, Qing Zhang, Rudolf Grosschedl, Zhiyong Yu, Jiong Deng, Yadi Wu

Summary: EBF1 is highly expressed in TNBC and plays a crucial role in tumorigenicity and progression; By forming a transcriptional complex with HIF1 alpha, EBF1 regulates cell mitophagy and prevents cell death; Targeting EBF1 pathway may offer alternative treatment strategies for TNBC.

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2022)

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Letter Medicine, General & Internal

Pembrolizumab in Early Triple-Negative Breast Cancer

Shuvadeep Ganguly, Ajay Gogia

Summary: In the KEYNOTE-522 trial, the addition of Pembrolizumab to neoadjuvant chemotherapy improved pathological complete response rate in early triple-negative breast cancer patients and also improved event-free survival. However, this improvement was predominantly observed in patients who did not achieve a pathological complete response.

NEW ENGLAND JOURNAL OF MEDICINE (2022)

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Article Oncology

Integrin αvβ6-TGFβ-SOX4 Pathway Drives Immune Evasion in Triple-Negative Breast Cancer

Archis Bagati, Sushil Kumar, Peng Jiang, Jason Pyrdol, Angela E. Zou, Anze Godicelj, Nathan D. Mathewson, Adam N. R. Cartwright, Paloma Cejas, Myles Brown, Anita Giobbie-Hurder, Deborah Dillon, Judith Agudo, Elizabeth A. Mittendorf, X. Shirley Liu, Kai W. Wucherpfennig

Summary: SOX4 transcription factor plays a key role in mediating resistance to T cell-mediated cytotoxicity in TNBC cells, and inhibiting it can increase the expression of genes in important immune pathways. The integrin αvβ6 receptor regulates the expression of SOX4, and targeting the integrin αvβ6-TGFβ-SOX4 pathway provides therapeutic opportunities for TNBC and other aggressive cancers of epithelial origin.

CANCER CELL (2021)

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Targeting CXCL16 and STAT1 augments immune checkpoint blockade therapy in triple-negative breast cancer

Bhavana Palakurthi, Shaneann R. Fross, Ian H. Guldner, Emilija Aleksandrovic, Xiyu Liu, Anna K. Martino, Qingfei Wang, Ryan A. Neff, Samantha M. Golomb, Cheryl Lewis, Yan Peng, Erin N. Howe, Siyuan Zhang

Summary: Chemotherapy priming enhances the response to immune checkpoint blockade in triple-negative breast cancers, but immune suppressive myeloid cells may hinder its efficacy. Through single-cell analysis, the authors characterize these immune suppressive myeloid cells and identify STAT1 signaling as a regulator of their suppressive state.

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A MXI1-NUTM1 fusion protein with MYC-like activity suggests a novel oncogenic mechanism in a subset ofNUTM1-rearranged tumors

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The androgen receptor is a tumor suppressor in estrogen receptor-positive breast cancer

Theresa E. Hickey, Luke A. Selth, Kee Ming Chia, Geraldine Laven-Law, Heloisa H. Milioli, Daniel Roden, Shalini Jindal, Mun Hui, Jessica Finlay-Schultz, Esmaeil Ebrahimie, Stephen N. Birrell, Suzan Stelloo, Richard Iggo, Sarah Alexandrou, C. Elizabeth Caldon, Tarek M. Abdel-Fatah, Ian O. Ellis, Wilbert Zwart, Carlo Palmieri, Carol A. Sartorius, Alex Swarbrick, Elgene Lim, Jason S. Carroll, Wayne D. Tilley

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Targeting the Hedgehog signalling pathway in triple negative breast cancer.

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