Energy metabolism pathways in breast cancer progression: The reprogramming, crosstalk, and potential therapeutic targets

Zheng, Xuewei; Ma, Haodi; Wang, Jingjing; Huang, Mengjiao; Fu, Dongliao; Qin, Ling; Yin, Qinan

doi:10.1016/j.tranon.2022.101534

Cited by 18 publications

(7 citation statements)

References 191 publications

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“…All these pathways contribute to breast cancer and metastasis. [35][36][37] For example, cell cycle is a valid therapeutic target in breast cancer. 35 Three different CDK4/6 inhibitors have been approved by the United States Food and Drug Administration for the treatment of hormone receptor-positive, human epidermal growth factor receptor 2-negative metastatic breast cancer.…”

Section: Discussionmentioning

confidence: 99%

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Mechanism of synergistic inhibitory effect of benzyl isothiocyanate and zoledronic acid combination on breast cancer induction of osteoclast differentiation

Hahm,

Kim,

Pore

et al. 2023

Molecular Carcinogenesis

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Bone is the most favored site for metastasis for each major subtype of breast cancer. Therapeutic modalities for alleviation of clinical symptoms associated with bone metastasis include surgical resection, radiation, and bone‐targeted therapies, including bisphosphonates (e.g., zoledronic acid; ZA) and a humanized antibody against receptor activator of nuclear factor‐κB ligand (denosumab). However, the bone‐targeted therapies are expensive, and have poor pharmacokinetic attributes and/or serious adverse effects. Therefore, novel strategies are needed for treatment of bone metastasis or to increase effectiveness of existing bone‐targeted therapies. We have shown previously that benzyl isothiocyanate (BITC) is a novel inhibitor of osteoclast differentiation in vitro and bone metastasis in vivo. The present study shows that BITC + ZA combination synergistically inhibits osteoclast differentiation induced by addition of conditioned media from breast cancer cells. These effects were associated with a significant increase in levels of several antiosteoclastogenic cytokines, including interferons, interleukin (IL)‐3, IL‐4, and IL‐27. Kyoto Encyclopedia of Genes and Genomes pathway analysis of RNA‐seq data from BITC and/or ZA‐treated cells revealed downregulation of genes of many pathways (e.g., actin cytoskeleton, Hippo signaling, etc.) by treatment with BITC + ZA combination, but not by BITC alone or ZA alone. Confocal microscopy confirmed severe disruption of actin cytoskeleton upon treatment of MCF‐7 and MDA‐MB‐231 cells with the BITC + ZA combination. This combination also decreased the nuclear level of yes‐associated protein, a core component of Hippo signaling. In conclusion, the present study offers a novel combination for prevention or treatment of bone metastasis of breast cancer.

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Section: Discussionmentioning

confidence: 99%

“…Genes associated with other cancer‐relevant pathways were also uniquely downregulated by the BITC + ZA combination, including cell cycle, citric acid cycle, and ribosomes (Figure 4). All these pathways contribute to breast cancer and metastasis 35–37 . For example, cell cycle is a valid therapeutic target in breast cancer 35 .…”

Section: Discussionmentioning

confidence: 99%

Mechanism of synergistic inhibitory effect of benzyl isothiocyanate and zoledronic acid combination on breast cancer induction of osteoclast differentiation

Hahm,

Kim,

Pore

et al. 2023

Molecular Carcinogenesis

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“…Like other tumor types, BC is accompanied by metabolic reprogramming required for the proliferation, growth, invasion and migration of BC cells [88]. Attri et al (2017) highlighted the racial disparity in the metabolic regulation of cancer [89].…”

Section: Metabolism-related Disparities In Breast Cancermentioning

confidence: 99%

Biological Basis of Breast Cancer-Related Disparities in Precision Oncology Era

Neagu,

Bruno,

Johnson

et al. 2024

IJMS

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Precision oncology is based on deep knowledge of the molecular profile of tumors, allowing for more accurate and personalized therapy for specific groups of patients who are different in disease susceptibility as well as treatment response. Thus, onco-breastomics is able to discover novel biomarkers that have been found to have racial and ethnic differences, among other types of disparities such as chronological or biological age-, sex/gender- or environmental-related ones. Usually, evidence suggests that breast cancer (BC) disparities are due to ethnicity, aging rate, socioeconomic position, environmental or chemical exposures, psycho-social stressors, comorbidities, Western lifestyle, poverty and rurality, or organizational and health care system factors or access. The aim of this review was to deepen the understanding of BC-related disparities, mainly from a biomedical perspective, which includes genomic-based differences, disparities in breast tumor biology and developmental biology, differences in breast tumors’ immune and metabolic landscapes, ecological factors involved in these disparities as well as microbiomics- and metagenomics-based disparities in BC. We can conclude that onco-breastomics, in principle, based on genomics, proteomics, epigenomics, hormonomics, metabolomics and exposomics data, is able to characterize the multiple biological processes and molecular pathways involved in BC disparities, clarifying the differences in incidence, mortality and treatment response for different groups of BC patients.

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“…The pathogenic mechanisms of BC are diverse, and the typical mechanism is metabolic reprogramming [ 2 ]. Profiting from the development of microarray and high-throughput sequencing technology, researchers can identify thousands of cancer-related genes and have innovative insights into their potential molecular mechanisms to apply them to fundamental research to benefit patients [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

The integration of multidisciplinary approaches revealed PTGES3 as a novel drug target for breast cancer treatment

Yin,

Ma,

Dong

et al. 2024

J Transl Med

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Background The main challenge in personalized treatment of breast cancer (BC) is how to integrate massive amounts of computing resources and data. This study aimed to identify a novel molecular target that might be effective for BC prognosis and for targeted therapy by using network-based multidisciplinary approaches. Methods Differentially expressed genes (DEGs) were first identified based on ESTIMATE analysis. A risk model in the TCGA-BRCA cohort was constructed using the risk score of six DEGs and validated in external and clinical in-house cohorts. Subsequently, independent prognostic factors in the internal and external cohorts were evaluated. Cell viability CCK-8 and wound healing assays were performed after PTGES3 siRNA was transiently transfected into the BC cell lines. Drug prediction and molecular docking between PTGES3 and drugs were further analyzed. Cell viability and PTGES3 expression in two BC cell lines after drug treatment were also investigated. Results A novel six-gene signature (including APOOL, BNIP3, F2RL2, HINT3, PTGES3 and RTN3) was used to establish a prognostic risk stratification model. The risk score was an independent prognostic factor that was more accurate than clinicopathological risk factors alone in predicting overall survival (OS) in BC patients. A high risk score favored tumor stage/grade but not OS. PTGES3 had the highest hazard ratio among the six genes in the signature, and its mRNA and protein levels significantly increased in BC cell lines. PTGES3 knockdown significantly inhibited BC cell proliferation and migration. Three drugs (gedunin, genistein and diethylstilbestrol) were confirmed to target PTGES3, and genistein and diethylstilbestrol demonstrated stronger binding affinities than did gedunin. Genistein and diethylstilbestrol significantly inhibited BC cell proliferation and reduced the protein and mRNA levels of PTGES3. Conclusions PTGES3 was found to be a novel drug target in a robust six-gene prognostic signature that may serve as a potential therapeutic strategy for BC.

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Energy metabolism pathways in breast cancer progression: The reprogramming, crosstalk, and potential therapeutic targets

Cited by 18 publications

References 191 publications

Mechanism of synergistic inhibitory effect of benzyl isothiocyanate and zoledronic acid combination on breast cancer induction of osteoclast differentiation

Mechanism of synergistic inhibitory effect of benzyl isothiocyanate and zoledronic acid combination on breast cancer induction of osteoclast differentiation

Biological Basis of Breast Cancer-Related Disparities in Precision Oncology Era

The integration of multidisciplinary approaches revealed PTGES3 as a novel drug target for breast cancer treatment

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