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BACKGROUND: The association between different phenotypes and genotypes of circulating tumor cells (CTCs) and efficacy of neoadjuvant chemotherapy (NAC) remains uncertain. This study was conducted to evaluate the relationship of FTH1 gene-associated CTCs (F-CTC) with/without epithelial-mesenchymal transition (EMT) markers, or their dynamic changes with the efficacy of NAC in patients with non-metastatic breast cancer. PATIENTS AND METHODS: This study enrolled 120 patients with non-metastatic breast cancer who planned to undergo NAC. The FTH1 gene and EMT markers in CTCs were detected before NAC (T0), after 2 cycles of chemotherapy (T1), and before surgery (T2). The associations of these different types of CTCs with rates of pathological complete response (pCR) and breast-conserving surgery (BCS) were evaluated using the binary logistic regression analysis. RESULTS: F-CTC in peripheral blood ≥1 at T0 was an independent factor for pCR rate in patients with HER2-positive (odds ratio [OR]=0.08, 95% confidence interval [CI], 0.01-0.98, P = .048). The reduction in the number of F-CTC at T2 was an independent factor for BCS rate (OR = 4.54, 95% CI, 1.14-18.08, P = .03). CONCLUSIONS: The number of F-CTC prior to NAC was related to poor response to NAC. Monitoring of F-CTC may help clinicians formulate personalized NAC regimens and implement BCS for patients with non-metastatic breast cancer.
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Neoplasias da Mama , Células Neoplásicas Circulantes , Humanos , Feminino , Neoplasias da Mama/tratamento farmacológico , Neoplasias da Mama/genética , Neoplasias da Mama/cirurgia , Células Neoplásicas Circulantes/patologia , Estudos Prospectivos , Terapia Neoadjuvante , Mastectomia Segmentar , Ferritinas/uso terapêutico , Oxirredutases/uso terapêuticoRESUMO
There is a wide variety of kinds of lipids, and complex structures which determine the diversity and complexity of their functions. With the basic characteristic of water insolubility, lipid molecules are independent of the genetic information composed by genes to proteins, which determine the particularity of lipids in the human body, with water as the basic environment and genes to proteins as the genetic system. In this review, we have summarized the current landscape on hormone regulation of lipid metabolism. After the well-studied PI3K-AKT pathway, insulin affects fat synthesis by controlling the activity and production of various transcription factors. New mechanisms of thyroid hormone regulation are discussed, receptor α and ß may mediate different procedures, the effect of thyroid hormone on mitochondria provides a new insight for hormones regulating lipid metabolism. Physiological concentration of adrenaline induces the expression of extrapituitary prolactin in adipose tissue macrophages, which promotes fat weight loss. Manipulation of hormonal action has the potential to offer a new therapeutic horizon for the global burden of obesity and its associated complications such as morbidity and mortality.
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Metabolismo dos Lipídeos , Prolactina , Humanos , Metabolismo dos Lipídeos/fisiologia , Prolactina/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Hormônios/metabolismo , Tecido Adiposo/metabolismo , Insulina/metabolismo , Hormônios Tireóideos/metabolismo , Epinefrina , Lipídeos , Fatores de Transcrição/metabolismo , Água/metabolismoRESUMO
As a noninvasive method, circulating tumor cell (CTC) provides ideal liquid biopsy specimens for early cancer screening and diagnosis. CTCs detection in breast cancer is correlated with patient prognosis such as disease-free survival (DFS) and overall survival (OS). Besides, accumulating evidence supported that CTCs count may be indicator for chemotherapy response as well. The functional roles of microRNA (miRNA) in breast cancer have been well-recognized for the last few years. Due to its stability in circulation, numerous studies have proven that circulating miRNA may serve as promising diagnostic and prognostic biomarkers in breast cancer. The potential ability of miRNAs in disease screening, staging or even molecular subtype classification makes them valuable tools for early breast cancer patients. It would be of great significance to characterize the miRNA expression profile in CTCs, which could provide reliable biological information originated from tumor. However, some issues need to be addressed before the utility of CTC-specific miRNAs in clinical setting. Taken together, we believe that CTC-specific miRNA detection will be trend for early breast cancer screening, diagnosis and treatment monitor in near future.
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Neoplasias da Mama , MicroRNAs , Células Neoplásicas Circulantes , Humanos , Feminino , Neoplasias da Mama/diagnóstico , Neoplasias da Mama/genética , Células Neoplásicas Circulantes/patologia , MicroRNAs/genética , Relevância Clínica , Intervalo Livre de DoençaRESUMO
Although the clinical application of nanoparticles is still limited by biological barriers and distribution, with the deepening of our understanding of nanoparticles over the past decades, people are gradually breaking through the previous limitations in the diagnosis and treatment of tumors, providing novel strategies for clinical decision makers. The transition of nanoparticles from passive targeting to active tumor-targeting by abundant surface-modified nanoparticles is also a development process of precision cancer treatment. Different particles can be used as targeted delivery tools of antitumor drugs. The mechanism of gold nanoparticles inducing apoptosis and cycle arrest of tumor cells has been discovered. Moreover, the unique photothermal effect of gold nanoparticles may be widely used in tumor therapy in the future, with less side effects on surrounding tissues. Lipid-based nanoparticles are expected to overcome the blood-brain barrier due to their special characteristics, while polymer-based nanoparticles show better biocompatibility and lower toxicity. In this paper, we discuss the development of nanoparticles in tumor therapy and the challenges that need to be addressed.
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Breast cancer is one of the leading causes of mortality in females. Over the past decades, intensive efforts have been made to uncover the pathogenesis of breast cancer. Interleukin-6 (IL-6) is a pleiotropic factor which has a vital role in host defense immunity and acute stress. Moreover, a wide range of studies have identified the physiological and pathological roles of IL-6 in inflammation, immune and cancer. Recently, several IL-6 signaling pathway-targeted monoclonal antibodies have been developed for cancer and immune therapy. Combination of IL-6 inhibitory antibody with other pathways blockage drugs have demonstrated promising outcome in both preclinical and clinical trials. This review focuses on emerging studies on the strong linkages of IL-6/IL-6R mediated regulation of inflammation and immunity in cancer, especially in breast cancer.
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Breast cancer is one the most common malignancies and leading cause of cancer-related mortality in women. Recent studies suggested that hypercholesterolemia may be the potential modifiable risk factors for breast cancer. Cholesterol was well-known for its strong association with cardiovascular disease for long. Moreover, solid evidence has been provided by different studies to illustrate the correlation between lipid and incidence in multiple cancers. Although the conclusion remains controversial or sometimes contrary, which may be due to the multifactorial nature of the disease and the disparity of ethnic population, it is critical to elucidate the relationship between specific cholesterol components in certain population and the exact underlying mechanism of the lipid-associated signaling pathway in breast cancer. The implications of dysregulated lipoproteins as therapeutic targets or options for breast cancer provide novel strategies for us in combating with this malignant disease, which may be achieved by manipulating lipid levels with pharmacological compounds.
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Neoplasias da Mama , Doenças Cardiovasculares , Hipercolesterolemia , Neoplasias da Mama/tratamento farmacológico , Doenças Cardiovasculares/epidemiologia , Colesterol/metabolismo , Colesterol/uso terapêutico , Feminino , Humanos , Hipercolesterolemia/tratamento farmacológico , Hipercolesterolemia/metabolismo , Fatores de RiscoRESUMO
PURPOSE: To explore the inhibition of proliferation and invasion of breast cancer cells by LncRNA SNHG7 via regulating the expression of miR-15a and its mechanism. METHODS: The expression of SNHG7 in breast cancer and adjacent tissues and different breast cancer cells was measured by qRT-PCR and the relationship between SNHG7 and clinicopathological parameters of breast cancer patients was analyzed. The interaction of SNHG7 with miR-15a was explored by dual-luciferase reporter assay. The change in the proliferation of breast cancer cells after silencing SNHG7 was examined by cell proliferation assay. The change in the invasion of breast cancer cells after silencing SNHG7 was examined by Transwell invasion assay. Subcutaneous tumor formation in nude mice was detected to record the tumor size and volume of tumor cells. RESULTS: Compared with adjacent normal tissues, the expression of SNHG7 was significantly increased in breast cancer tissues; the expression of SNHG7 was the highest in breast cancer cells MCF7 and T47D; the expression level of SNHG7 was not notably different among breast cancer patients of different genders and age groups, and the difference was not statistically significant (p>0.05). The expression level of SNHG7 was higher in patients with a higher stage of breast cancer and patients with lymph node metastasis, and the difference was statistically significant. SNHG7 could specifically bind to the 3' UTR of miR-15a. The inhibition of SNHG7 led to constrained proliferation and invasion of breast cancer cells. The tumor volume and weight of the tumor-bearing mice in the si-SNHG7 group were significantly lower than those in the non-specific control (NC) group. CONCLUSION: SNHG7 plays an important role in the development of breast cancer. SNHG7 can affect the proliferation and invasion of breast cancer cells through its targeted regulation of miR-15a activity.