Reversal of epithelial-mesenchymal transition and inhibition of tumor stemness of breast cancer cells through advanced combined chemotherapy

Cui, Yani; Zhao, Mingda; Yang, Yuedi; Xu, Ruiling; Tong, Lei; Liang, Jie; Zhang, Xingdong; Sun, Yong; Fan, Yujiang

doi:10.1016/j.actbio.2022.08.024

Cited by 16 publications

(8 citation statements)

References 47 publications

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“…Specifically, the presence of the CSCs has been associated with resistance to chemotherapeutic agents such as cisplatin, bortezomib, etoposide, 5-FU, and doxorubicin [ 92 , 96 ] . Most importantly, many studies have demonstrated that treatment with these drugs enhances the CSCs fraction in different solid tumors and favors EMT traits, leading to treatment resistance and cancer progression [ 97 , 98 ] . In addition, the acquisition of resistance to a specific drug generally tends to multiply resistance to unrelated compounds in CSCs and malignant cells, which under treatment pressure, can acquire a stem-like phenotype and become therapeutic resistant [ 18 ] .…”

Section: Chemotherapy Resistance and Cscmentioning

confidence: 99%

Mechanisms involved in cancer stem cell resistance in head and neck squamous cell carcinoma

Siqueira¹,

Heguedusch²,

Rodini³

et al. 2023

Cancer Drug Resist

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Despite scientific advances in the Oncology field, cancer remains a leading cause of death worldwide. Molecular and cellular heterogeneity of head and neck squamous cell carcinoma (HNSCC) is a significant contributor to the unpredictability of the clinical response and failure in cancer treatment. Cancer stem cells (CSCs) are recognized as a subpopulation of tumor cells that can drive and maintain tumorigenesis and metastasis, leading to poor prognosis in different types of cancer. CSCs exhibit a high level of plasticity, quickly adapting to the tumor microenvironment changes, and are intrinsically resistant to current chemo and radiotherapies. The mechanisms of CSC-mediated therapy resistance are not fully understood. However, they include different strategies used by CSCs to overcome challenges imposed by treatment, such as activation of DNA repair system, anti-apoptotic mechanisms, acquisition of quiescent state and Epithelial-mesenchymal transition, increased drug efflux capacity, hypoxic environment, protection by the CSC niche, overexpression of stemness related genes, and immune surveillance. Complete elimination of CSCs seems to be the main target for achieving tumor control and improving overall survival for cancer patients. This review will focus on the multi-factorial mechanisms by which CSCs are resistant to radiotherapy and chemotherapy in HNSCC, supporting the use of possible strategies to overcome therapy failure.

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Section: Chemotherapy Resistance and Cscmentioning

confidence: 99%

Mechanisms involved in cancer stem cell resistance in head and neck squamous cell carcinoma

Siqueira¹,

Heguedusch²,

Rodini³

et al. 2023

Cancer Drug Resist

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“…Erastin not only improved the intracellular accumulation of DOX by inhibiting its efflux but also amplified the oxidative stress induced by DOX in cancer cells and CSCs . In addition, the combined delivery of chemotherapeutic agents such as salinomycin (SAL) and DOX, SAL and the active form of irinotecan SN38 using nanomaterials has demonstrated great achievements in enhancing therapeutic efficacy.…”

Section: Strategies For Sniping Cscsmentioning

confidence: 99%

Sniping Cancer Stem Cells with Nanomaterials

Wang,

Guo,

Yang

et al. 2023

ACS Nano

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“…Wnt/β-catenin signaling serves a key role in EMT in tumor cells (80)(81)(82). Wnt is a secreted glycoprotein that interacts with specific receptors on the cell surface through autocrine and paracrine mechanisms and induces the accumulation of β-catenin through phosphorylation and dephosphorylation of downstream proteins.…”

Section: Usp2 Promotes Emt and Enhances The Migratory And Invasive Ca...mentioning

confidence: 99%

Targeting the deubiquitinase USP2 for malignant tumor therapy (Review)

Zhang,

Guo,

Zhang

et al. 2023

Oncol Rep

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The ubiquitin-proteasome system is a major degradation pathway for >80% of proteins in vivo. Deubiquitylases, which remove ubiquitinated tags to stabilize substrate proteins, are important components involved in regulating the degradation of ubiquitinated proteins. In addition, they serve multiple roles in tumor development by participating in physiological processes such as protein metabolism, cell cycle regulation, DNA damage repair and gene transcription. The present review systematically summarized the role of ubiquitin-specific protease 2 (USP2) in malignant tumors and the specific molecular mechanisms underlying the involvement of USP2 in tumor-associated pathways. USP2 reverses ubiquitin-mediated degradation of proteins and is involved in aberrant proliferation, migration, invasion, apoptosis and drug resistance of tumors. Additionally, the present review summarized studies reporting on the use of USP2 as a therapeutic target for malignancies such as breast, liver, ovarian, colorectal, bladder and prostate cancers and glioblastoma and highlights the current status of pharmacological research on USP2. The clinical significance of USP2 as a therapeutic target for malignant tumors warrants further investigation. Contents 1. Introduction 2. Role of USP2 in the biological behavior of malignant tumors 3. Targeting USP2 for cancer therapy 4. Pharmacological studies of USP2 5. Concluding remarks and potential future directions

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Reversal of epithelial-mesenchymal transition and inhibition of tumor stemness of breast cancer cells through advanced combined chemotherapy

Cited by 16 publications

References 47 publications

Mechanisms involved in cancer stem cell resistance in head and neck squamous cell carcinoma

Mechanisms involved in cancer stem cell resistance in head and neck squamous cell carcinoma

Sniping Cancer Stem Cells with Nanomaterials

Targeting the deubiquitinase USP2 for malignant tumor therapy (Review)

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