Progress of Breast Cancer basic research in China

Wang, Xuerong; Wang, Chao; Guan, Jiaheng; Chen, Baoan; Xu, Lin; Chen, Ceshi

doi:10.7150/ijbs.60631

Cited by 71 publications

(39 citation statements)

References 101 publications

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“…It is regarded as a diverse and heterogeneous disease with different phenotypes, prognoses, and responses to treatment 4–6 . Statistics show that breast cancer accounts for 30% of female’s newly diagnosed cancer cases and 15% of female’s cancer deaths 7 , 8 . It is estimated that there are 1 million confirmed cases of breast cancer each year all over the world.…”

Section: Introductionmentioning

confidence: 99%

Design and synthesis of chromone-nitrogen mustard derivatives and evaluation of anti-breast cancer activity

Sun

Wang

et al. 2021

Journal of Enzyme Inhibition and Medicinal Chemistry

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Chromone has emerged as one of the most important synthetic scaffolds for antitumor activity, which promotes the development of candidate drugs with better activity. In this study, a series of nitrogen mustard derivatives of chromone were designed and synthesised, in order to discover promising anti-breast tumour candidates. Almost all target derivatives showed antiproliferative activity against MCF-7 and MDA-MB-231 cell lines. In particular, methyl ( S )-3-(4-(bis(2-chloroethyl)amino)phenyl)-2-(5-(((6-methoxy-4-oxo-4 H -chromen-3-yl)methyl)amino)-5-oxopentanamido)propanoate showed the most potent antiproliferative activity with IC 50 values of 1.83 and 1.90 μM, respectively, and it also exhibited certain selectivity between tumour cells and normal cells. Further mechanism exploration against MDA-MB-231 cells showed that it possibly induced G2/M phase arrest and apoptosis by generating intracellular ROS and activating DNA damage. In addition, it also inhibited MDA-MB-231 cells metastasis, invasion and adhesion. Overall, methyl ( S )-3-(4-(bis(2-chloroethyl)amino)phenyl)-2-(5-(((6-methoxy-4-oxo-4 H -chromen-3-yl)methyl)amino)-5-oxopentanamido)propanoate showed potent antitumor activities and relatively low side effects, and deserved further investigation.

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Section: Introductionmentioning

confidence: 99%

Design and synthesis of chromone-nitrogen mustard derivatives and evaluation of anti-breast cancer activity

Sun

Wang

et al. 2021

Journal of Enzyme Inhibition and Medicinal Chemistry

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“…Cell migration and invasion were determined by wound-healing and transwell assays as described previously 6 , 12 .…”

Section: Methodsmentioning

confidence: 99%

“…Oncogenes, growth factors, inflammatory factors and cancer microenvironment may jointly promote cancer metastasis by enhancing cancer cell motility, invasion, colonization and angiogenesis 1 - 5 . A better understanding the mechanisms of cancer metastasis may help uncover novel biomarkers and therapeutic targets 6 .…”

Section: Introductionmentioning

confidence: 99%

Gamma synuclein promotes cancer metastasis through the MKK3/6-p38MAPK cascade

Liu¹,

Shao²,

Zhang³

et al. 2022

Int. J. Biol. Sci.

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Gamma synuclein (SNCG) is a neuronal protein that is also aberrantly overexpressed in various types of human cancer. SNCG overexpression promotes cancer invasion and metastasis. However, the mechanisms that drive cancer metastasis upon SNCG expression remain elusive. Elucidation of the mechanisms underlying the promotion of cancer metastasis by SNCG may help discover therapeutic avenues for SNCG-overexpressed cancer. Here, we show that SNCG promotes transforming growth factor-β (TGF-β)-induced p38 mitogen-activated protein kinase (MAPK) phosphorylation. Mechanistically, SNCG promotes p38MAPK phosphorylation by interacting with the MAPK kinase 3/6 (MKK3/6) and prevents their degradation. SNCG knockdown leads to a decrease in TGF-β-induced phosphorylation of MKK3/6; and abrogates the induction of matrix metalloproteinase (MMP)-9 expression by TGF-β and its target gene Twist1. Furthermore, p38MAPK inhibition abrogates the promotion of MMP-9 expression and cancer cell invasion by SNCG. Both p38MAPK and MMP inhibitors can suppress the promotion of cancer cell invasion by SNCG. Finally, overexpression of SNCG in liver cancer cells promotes lung metastasis, which can be suppressed by the p38MAPK inhibitor. Together, our data uncover a previously unknown role of SNCG in promoting TGF-β-MKK3/6-p38MAPK signaling. This study highlights the critical role of p38MAPK in the promotion of cancer metastasis by SNCG, and indicates that p38MAPK inhibitor may serve as a potential therapeutic for SNCG-overexpressed cancer.

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“…Breast cancer is the most familiar malignancy in Chinese women and the sixth main cause of cancer-related death ( 1 ). By the end of 2008, 169,452 new breast cancer cases were reported in China; 44,908 cases were related deaths ( 2 ).…”

Section: Introductionmentioning

confidence: 99%

The COMT Genetic Factor Regulates Chemotherapy-Related Prospective Memory Impairment in Survivors With HER2−/+ Breast Cancer

Zhang

Cai

et al. 2022

Front. Oncol.

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BackgroundPrevious findings indicated that polymorphism in gene catechol-O-methyltransferase (COMT) had been linked to chemotherapy-related cognitive impairment (CRCI). Nevertheless, the motivation of COMT polymorphisms in regulating cognitive impairment in breast cancer survivors with disparate status of human epidermal growth factor receptor 2 (HER2) was still vague.ObjectiveThe current research aimed to evaluate the regulation of the risk by COMT genotype on CRCI in breast cancer survivors with disparate status of HER2.MethodsBreast cancer survivors (103 with HER2− and 118 with HER2+) underwent neuropsychological tests before and after chemotherapy, containing event- and time-based prospective memory (EBPM and TBPM). Three single-nucleotide polymorphisms (SNPs) were estimated by providing peripheral blood, containing COMT (rs165599, rs737865, and rs4680).ResultsThe EBPM and TBPM performances was lower as compared with these before chemotherapy (z = −7.712, z = −2.403, respectively, p < 0.01). Furthermore, the EBPM and TBPM performances of HER2− group survivors were lower than those of HER2+ group survivors after chemotherapy (z = −7.181, p < 0.01; z = −2.205 p < 0.05, respectively). The survivors with COMT (rs165599) A/A genotype carriers had a meaningfully poorer chance of memory descend [dominant model: adjusted, OR = 2.21, CI (95%) = 1.156–4.225, p = 0.016] and showed better on TBPM test, relative to G/G genotype. Patients with the COMT (rs737865) A/G and G/G genotype showed protective function than the patients with the A/A and performed better on MMSE and TBPM tests.ConclusionThe types of HER2 may be correlated to chemotherapy-related prospective memory impairments in breast cancer survivors. Furthermore, the COMT (rs165599, rs737865) polymorphisms were correlated to the risk of TBPM decline scores and possibly be a potential genetic identifying for increasing risk of CRCI in breast cancer patients with disparate status of HER2.

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Progress of Breast Cancer basic research in China

Cited by 71 publications

References 101 publications

Design and synthesis of chromone-nitrogen mustard derivatives and evaluation of anti-breast cancer activity

Design and synthesis of chromone-nitrogen mustard derivatives and evaluation of anti-breast cancer activity

Gamma synuclein promotes cancer metastasis through the MKK3/6-p38MAPK cascade

The COMT Genetic Factor Regulates Chemotherapy-Related Prospective Memory Impairment in Survivors With HER2−/+ Breast Cancer

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