Global incidence and mortality of breast cancer: a trend analysis

Huang, Junjie; Chan, Paul; Lok, Veeleah; Chen, Xiao; Ding, Hanyue; Jin, Yinzi; Yuan, Jinqiu; Lao, Xiang Qian; Zheng, Zhi‐Jie; Wong, Martin Cs

doi:10.18632/aging.202502

Cited by 144 publications

(79 citation statements)

References 37 publications

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“…In the last decade, the global incidence of BC has shown an increasing trend with no significant reduction in mortality [21,22]. Patients with early, locally advanced, and locally recurrent BC are considered to have a higher chance of cure.…”

Section: Breast Cancer and Targeted Therapymentioning

confidence: 99%

Key Factor Regulating Inflammatory Microenvironment, Metastasis, and Resistance in Breast Cancer: Interleukin-1 Signaling

Liu

Lan

et al. 2021

Mediators of Inflammation

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Breast cancer is one of the top-ranked cancers for incidence and mortality worldwide. The biggest challenges in breast cancer treatment are metastasis and drug resistance, for which work on molecular evaluation, mechanism studies, and screening of therapeutic targets is ongoing. Factors that lead to inflammatory infiltration and immune system suppression in the tumor microenvironment are potential therapeutic targets. Interleukin-1 is known as a proinflammatory and immunostimulatory cytokine, which plays important roles in inflammatory diseases. Recent studies have shown that interleukin-1 cytokines drive the formation and maintenance of an inflammatory/immunosuppressive microenvironment through complex intercellular signal crosstalk and tight intracellular signal transduction, which were found to be potentially involved in the mechanism of metastasis and drug resistance of breast cancer. Some preclinical and clinical treatments or interventions to block the interleukin-1/interleukin-1 receptor system and its up- and downstream signaling cascades have also been proven effective. This study provides an overview of IL-1-mediated signal communication in breast cancer and discusses the potential of IL-1 as a therapeutic target especially for metastatic breast cancer and combination therapy and current problems, aiming at enlightening new ideas in the study of inflammatory cytokines and immune networks in the tumor microenvironment.

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Section: Breast Cancer and Targeted Therapymentioning

confidence: 99%

Key Factor Regulating Inflammatory Microenvironment, Metastasis, and Resistance in Breast Cancer: Interleukin-1 Signaling

Liu

Lan

et al. 2021

Mediators of Inflammation

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“…Breast cancer is one of the most frequently diagnosed malignancies among women ( 1 ). During the past few decades, the incidence of breast cancer has continued to increase, and a total of 2,088,849 newly diagnosed cases of breast cancer were reported in 2018 worldwide ( 2 , 3 ). The majority of patients with breast cancer are curable at the non-metastatic stage; however, current therapeutics exhibit minimal efficacy against advanced-stage metastatic disease.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑301a‑3p promotes triple‑negative breast cancer progression through downregulating MEOX2

Liu

Wang

2021

Exp Ther Med

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Breast cancer is one of the most frequently diagnosed malignancies among women. Triple-negative breast cancer (TNBC) represents a significant challenge for breast oncologists, as the availability of effective therapies for this aggressive disease is limited. The molecular mechanisms underlying TNBC development are not fully understood. Previous studies have demonstrated that microRNAs (miRNAs/miRs) play important roles in the development of various types of cancer, including breast cancer; however, the role of miRNAs in TNBC remains undetermined. The results of the present study revealed that miR-301a-3p may function as an oncogenic miRNA in TNBC. Based on The Cancer Genome Atlas data, miR-301a-3p expression levels were found to be upregulated in breast cancer tissues. Reverse transcription-quantitative PCR analysis demonstrated that the expression levels of miR-301a-3p were upregulated in TNBC tissues compared with non-TNBC tissues, and in MDA-MB-231 cells compared with normal MCF-10A breast cells. miR-301a-3p mimics and inhibitors were subsequently used to overexpress and knock down miR-301a-3p expression, respectively, in MDA-MB-231 cells. Biological functional experiments demonstrated that miR-301a-3p overexpression increased the viability, and the migratory and invasive abilities of MDA-MB-231 cells. By contrast, miR-301a-3p knockdown exerted the opposite effects on MDA-MB-231 cells. Cell apoptosis was negatively regulated by miR-301a-3p. Moreover, overexpression of miR-301a-3p was found to downregulate the expression levels of mesenchyme homeobox 2 (MEOX2). The expression levels of miR-301a-3p were negatively correlated with the expression levels of MEOX2 in clinical tissue specimens from patients with TNBC. Subsequently, the knockdown of MEOX2 expression promoted the viability of MDA-MB-231 cells. In conclusion, the results of the present study suggested that miR-301a-3p may serve as an oncogenic miRNA in TNBC by regulating MEOX2 expression.

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“…Furthermore, research studies have reported that a large number of countries showed a rapidly rising incidence. Additionally, the incidence of breast cancers tends to be younger (Huang et al, 2021). Nowadays, chemotherapy is one of the most commonly used clinical treatments for breast cancers, which can effectively inhibit the growth of cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of fucoidan on breast cancer cells and potential enhancement of their sensitivity to chemotherapy by regulating autophagy

Zhang

Xue

Wang

et al. 2021

Phytotherapy Research

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Fucoidan is a marine‐origin sulfated polysaccharide that has gained attention for its anticancer activities. However, the inhibitory effect of fucoidan on breast cancers by regulating autophagy and its mechanism are not clear, and the chemotherapeutic sensitization of fucoidan is largely unknown. In the present study, the anticancer potential of fucoidan was revealed in MCF‐7 and MDA‐MB‐231 cells. Additionally, we also studied the chemotherapeutic sensitization of fucoidan by combining chemotherapeutic drugs doxorubicin (ADM) and cisplatin (DDP) with fucoidan on breast cancer cells. In the two kinds of human breast cancer cells, cell viability was determined by 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide (MTT) assay. Apoptosis was examined with flow cytometry. Transfection assay was used to examine autophagy flow. Western blot was used to examine the expressions of related proteins. Results suggested that fucoidan could induce autophagy and might enhance the sensitivity of breast cancer cells to chemotherapeutic drugs. Mechanistically, fucoidan induced autophagy in breast cancer cells by down‐regulating m‐TOR/p70S6K/TFEB pathway. In conclusion, our research revealed that fucoidan could induce autophagy of breast cancer cells by mediating m‐TOR/p70S6K/TFEB pathway, thus inhibiting tumor development. Furthermore, fucoidan might enhance the sensitivity of breast cancer cells to ADM and DDP, and this enhancement was related to autophagy.

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Global incidence and mortality of breast cancer: a trend analysis

Cited by 144 publications

References 37 publications

Key Factor Regulating Inflammatory Microenvironment, Metastasis, and Resistance in Breast Cancer: Interleukin-1 Signaling

Key Factor Regulating Inflammatory Microenvironment, Metastasis, and Resistance in Breast Cancer: Interleukin-1 Signaling

MicroRNA‑301a‑3p promotes triple‑negative breast cancer progression through downregulating MEOX2

Inhibition of fucoidan on breast cancer cells and potential enhancement of their sensitivity to chemotherapy by regulating autophagy

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