Tumor-promoting aftermath post-chemotherapy: A focus on breast cancer

Famta, Paras; Shah, Saurabh; Jain, Naitik; Kumar, Kondasingh Charan; Bagasariya, Deepkumar; Khatri, Dharmendra Kumar; Raghuvanshi, Rajeev Singh; Singh, Shashi Bala; Srivastava, Saurabh

doi:10.1016/j.lfs.2022.121125

Cited by 21 publications

(7 citation statements)

References 145 publications

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“…The tumor-promoting effect of chemotherapy was previously named "treatment backfire" [137], and its mechanisms have been recently discussed in detail [138,139]. On the other side, cytostatic therapies (including molecularly targeted drugs and low-dose chemotherapeutic regimens) usually achieve a temporary regression/stabilization of responsive tumors, inducing less drastic changes both in the tumor and in the TME.…”

Section: Cancer-immune System Interactions Involved In Quiescencementioning

confidence: 99%

Dormancy, stemness, and therapy resistance: interconnected players in cancer evolution

Francescangeli

Angelis

Rossi

et al. 2023

Cancer Metastasis Rev

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The biological complexity of cancer represents a tremendous clinical challenge, resulting in the frequent failure of current treatment protocols. In the rapidly evolving scenario of a growing tumor, anticancer treatments impose a drastic perturbation not only to cancer cells but also to the tumor microenvironment, killing a portion of the cells and inducing a massive stress response in the survivors. Consequently, treatments can act as a double-edged sword by inducing a temporary response while laying the ground for therapy resistance and subsequent disease progression. Cancer cell dormancy (or quiescence) is a central theme in tumor evolution, being tightly linked to the tumor’s ability to survive cytotoxic challenges, metastasize, and resist immune-mediated attack. Accordingly, quiescent cancer cells (QCCs) have been detected in virtually all the stages of tumor development. In recent years, an increasing number of studies have focused on the characterization of quiescent/therapy resistant cancer cells, unveiling QCCs core transcriptional programs, metabolic plasticity, and mechanisms of immune escape. At the same time, our partial understanding of tumor quiescence reflects the difficulty to identify stable QCCs biomarkers/therapeutic targets and to control cancer dormancy in clinical settings. This review focuses on recent discoveries in the interrelated fields of dormancy, stemness, and therapy resistance, discussing experimental evidences in the frame of a nonlinear dynamics approach, and exploring the possibility that tumor quiescence may represent not only a peril but also a potential therapeutic resource.

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Section: Cancer-immune System Interactions Involved In Quiescencementioning

confidence: 99%

Dormancy, stemness, and therapy resistance: interconnected players in cancer evolution

Francescangeli

Angelis

Rossi

et al. 2023

Cancer Metastasis Rev

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“…Of note, a correlation of an increased level of ABC transporters with evasion of apoptosis, an increase in cell migration to provide the potential for invasion and metastasis, resulting in tumor aggressiveness has been reported (Fletcher et al 2010;Zhang et al 2014;Pote and Gacche 2023) As a result of epithelial-mesenchymal transition (EMT), epithelial-derived carcinoma cells undergo a reversible process involving changes in cell-to-cell adhesion and polarity, cytoskeletal remodeling, enhanced migration and invasiveness, and dissemination to secondary organs; therefore, it is regarded as a pivotal process during cancer progression (Christofori 2006;Thiery and Sleeman 2006;Liu et al 2013;Zheng and Kang 2014;Nieto et al 2016). Of note, EMT has been reported to confer characteristics of drug resistance against several conventional therapeutic agents in human pancreatic cell lines, and against EG-FR-targeted therapies in lung cancer (Fuchs et al 2008;Sabbah et al 2008;Arumugam et al 2009;Abotaleb et al 2018;Famta et al 2022). Similar studies have also reported that an active EMT phenomenon in breast cancer cell lines renders them unresponsive to treatment with tamoxifen, paclitaxel, and adriamycin (Kang and Massagué 2004;Peinado et al 2004;De Craene et al 2005).…”

Section: Drug Targets and Therapeuticsmentioning

confidence: 99%

“…Breast cancer, the most commonly diagnosed cancer in women, is the leading cause of cancer-related death (Shi et al 2013;Yu et al 2014;Famta et al 2022). The application of multidisciplinary treatments that include surgery, hormonal therapy, radiation, and chemotherapy for patients with breast cancer has been reported (Prihantono and Faruk 2021).…”

Section: Introductionmentioning

confidence: 99%

“…The application of multidisciplinary treatments that include surgery, hormonal therapy, radiation, and chemotherapy for patients with breast cancer has been reported (Prihantono and Faruk 2021). Among these, chemotherapy is still regarded as a major approach in the treatment of breast cancer (Famta et al 2022). In particular, neoadjuvant chemotherapy, which has become the standard protocol for the management of locally advanced breast cancer, is the preferred treatment for operable breast cancer at an early stage.…”

Section: Introductionmentioning

confidence: 99%

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EMT-Activating Transcription Factor Slug is Involved in the Phenotypic Change as Well as Drug Sensitivity in Adriamycin- Resistant MCF-7 Cells

Kim

Jung

2023

DTT

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Adriamycin is currently used in the treatment of breast cancer, however, acquired resistance to adriamycin is a critical problem. This study examined the gene expression involved in resistance to adriamycin in MCF-7 breast cancer cells, with a particular focus on the epithelial-mesenchymal transition (EMT). The level of E-cadherin, an epithelial marker, was significantly decreased, however, an obvious increase was observed in the levels of mesenchymal markers in adriamycin-resistant MCF-7 (MCF-7/ADR) cells, implying that EMT is induced by adriamycin resistance. In the evaluation of target transcription factors involved in EMT, Slug is predominantly expressed in MCF-7/ADR cells. Knockdown of Slug in MCF-7/ ADR cells resulted in significant recovery of the epithelial characteristics. Of particular significance, the downregulation of Slug using siRNA resulted in repressed P-glycoprotein (P-gp) as well as increased sensitivity to adriamycin. Taken together, these findings suggest the potential importance of Slug in the acquisition of mesenchymal characteristics as well as the expression of P-gp in adriamycin-resistant MCF-7 cells.

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“…MDR is due in part to robust expression of the ABCG2 efflux protein, also known as Breast Cancer Resistance Protein (BCRP) ( Zhou et al, 2001 ; Zattoni et al, 2022 ), a direct transcriptional target of AhR ( Tan et al, 2010 ). Substantial efforts have focused on strategies which will lead to the effective elimination of BCSCs, however it is recognized that standard endocrine and chemotherapy regimens paradoxically enrich for BCSCs with mesenchymal features, driving tumor recurrence ( Li et al, 2008 ; Creighton et al, 2009 ; Famta et al, 2022 ).…”

Section: The Intersection Between Environmental Exposure and Cancer S...mentioning

confidence: 99%

Environmental exposure and the role of AhR in the tumor microenvironment of breast cancer

2022

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Activation of the aryl hydrocarbon receptor (AhR) through environmental exposure to chemicals including polycyclic aromatic hydrocarbons (PAHs) and polychlorinated dibenzo-p-dioxins (PCDDs) can lead to severe adverse health effects and increase the risk of breast cancer. This review considers several mechanisms which link the tumor promoting effects of environmental pollutants with the AhR signaling pathway, contributing to the development and progression of breast cancer. We explore AhR’s function in shaping the tumor microenvironment, modifying immune tolerance, and regulating cancer stemness, driving breast cancer chemoresistance and metastasis. The complexity of AhR, with evidence for both oncogenic and tumor suppressor roles is discussed. We propose that AhR functions as a “molecular bridge”, linking disproportionate toxin exposure and policies which underlie environmental injustice with tumor cell behaviors which drive poor patient outcomes.

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Tumor-promoting aftermath post-chemotherapy: A focus on breast cancer

Cited by 21 publications

References 145 publications

Dormancy, stemness, and therapy resistance: interconnected players in cancer evolution

Dormancy, stemness, and therapy resistance: interconnected players in cancer evolution

EMT-Activating Transcription Factor Slug is Involved in the Phenotypic Change as Well as Drug Sensitivity in Adriamycin- Resistant MCF-7 Cells

Environmental exposure and the role of AhR in the tumor microenvironment of breast cancer

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