A pilot trial of neoadjuvant pyrotinib plus trastuzumab, dalpiciclib, and letrozole for triple-positive breast cancer.

Triple-positive breast cancer (TPBC) poorly responds to current standard neoadjuvant therapy (trastuzumab plus pertuzumab and chemotherapy). Our previous MUKDEN 01 study showed a promising total pathological complete response (tpCR) rate of 30.4% with neoadjuvant pyrotinib (pan-human epidermal growth factor receptor tyrosine kinase inhibitor) plus dalpiciclib (cyclin-dependent kinase 4/6 inhibitor) and letrozole, but the efficacy remains suboptimal. This pilot study (NCT05228951) explored adding trastuzumab to this triplet neoadjuvant regimen in patients with stage II-III TPBC. The primary endpoint was tpCR (ypT0/is, ypN0) rate. Between February 2022 and June 2022, 12 patients were enrolled, and seven (58%; 95% confidence interval [CI], 27.7%-84.8%) patients achieved tpCR. The rate of residual cancer burden (RCB) 0-I was 75% (95% CI, 46.8%-91.1%). The objective response rate (ORR) was 92% (95% CI, 64.6%-98.5%). Mean Ki-67 level was significantly reduced from 45.0% (95% CI, 19.5%-70.5%) at baseline to 17.2% (95% CI, 0.7%-33.7%) after neoadjuvant therapy (p = 0.03). The most common grade 3 adverse events were diarrhea (four [33%]) and decreased neutrophil count (three [25%]). No grade 4 adverse events or treatment-related deaths occurred. This four-drug neoadjuvant regimen shows promising pathological response with an acceptable safety profile in patients with TPBC. A randomized controlled trial (NCT05638594) of this regimen is being conducted.

Predicting the Survival Benefit of Radiotherapy in Elderly Breast Cancer Patients: A Population-Based Analysis.

INTRODUCTION: This study aimed to establish two prediction tools predicting cancer-specific survival (CSS) and overall survival (OS) in elderly breast cancer patients with or without radiotherapy. METHODS: Clinicopathological data of breast cancer patients aged more than 70 y from 2010 to 2018 were retrospectively collected from the Surveillance, Epidemiology, and End Results database. Patients were randomly divided into the training and validation cohorts at 7:3, and the Cox proportional risk model was used to construct the nomograms. The concordance index, the area under the receiver operating characteristic curve, and the calibration plot are used to evaluate the discrimination and accuracy of the nomograms. RESULTS: One lakh twenty eight thousand two hundred twenty three elderly breast cancer patients were enrolled, including 57,915 who received radiotherapy. The Cox regression model was used to identify independent factors. These independent influencing factors are used to construct the prediction models. The calibration plots reflect the excellent consistency between the predicted and actual survival rates. The concordance index of nomograms for CSS and OS was more than 0.7 in both the radiotherapy group and the nonradiotherapy group, and similar results are also shown in area under the receiver operating characteristic curve. Decision curve analysis showed that the prognostication accuracy of the model was much higher than that of the traditional tumor, node, metastasis staging. CONCLUSIONS: Radiotherapy can benefit elderly breast cancer patients significantly. The two prediction tools provide a personalized survival scale for evaluating the CSS and OS of elderly breast cancer patients, which can better provide clinicians with better-individualized management for these patients.

A prognostic mathematical model based on tumor microenvironment-related genes expression for breast cancer patients.

Background: Tumor microenvironment (TME) status is closely related to breast cancer (BC) prognosis and systemic therapeutic effects. However, to date studies have not considered the interactions of immune and stromal cells at the gene expression level in BC as a whole. Herein, we constructed a predictive model, for adjuvant decision-making, by mining TME molecular expression information related to BC patient prognosis and drug treatment sensitivity. Methods: Clinical information and gene expression profiles were extracted from The Cancer Genome Atlas (TCGA), with patients divided into high- and low-score groups according to immune/stromal scores. TME-related prognostic genes were identified using Kaplan-Meier analysis, functional enrichment analysis, and protein-protein interaction (PPI) networks, and validated in the Gene Expression Omnibus (GEO) database. Least absolute shrinkage and selection operator (LASSO) Cox regression analysis was used to construct and verify a prognostic model based on TME-related genes. In addition, the patients' response to chemotherapy and immunotherapy was assessed by survival outcome and immunohistochemistry (IPS). Immunohistochemistry (IHC) staining laid a solid foundation for exploring the value of novel therapeutic target genes. Results: By dividing patients into low- and high-risk groups, a significant distinction in overall survival was found (p < 0.05). The risk model was independent of multiple clinicopathological parameters and accurately predicted prognosis in BC patients (p < 0.05). The nomogram-integrated risk score had high prediction accuracy and applicability, when compared with simple clinicopathological features. As predicted by the risk model, regardless of the chemotherapy regimen, the survival advantage of the low-risk group was evident in those patients receiving chemotherapy (p < 0.05). However, in patients receiving anthracycline (A) therapy, outcomes were not significantly different when compared with those receiving no-A therapy (p = 0.24), suggesting these patients may omit from A-containing adjuvant chemotherapy. Our risk model also effectively predicted tumor mutation burden (TMB) and immunotherapy efficacy in BC patients (p < 0.05). Conclusion: The prognostic score model based on TME-related genes effectively predicted prognosis and chemotherapy effects in BC patients. The model provides a theoretical basis for novel driver-gene discover in BC and guides the decision-making for the adjuvant treatment of early breast cancer (eBC).

Anti-obesity effects exerted by Dioscorea opposita Thunb. polysaccharides in diet-induced obese mice.

Obesity is characterized by chronic inflammation, insulin resistance, and gut microbiota dysbiosis. Dioscorea opposita Thunb. is a traditional food and medicine homolog from China. In the present study, polysaccharides isolated from a water extract of Dioscorea opposita Thunb. (DOTPs) were prepared. We showed that DOTPs reduced body weight, accumulation of fat tissues, insulin resistance, and inflammation in high-fat diet (HFD)-fed mice. Further experiments showed that DOTPs could regulate the composition of the gut microbiota in HFD mice. DOTPs supplementation in HFD-fed mice resulted in the reduction of the Firmicutes-to-Bacteroidetes ratio. We further demonstrated that DOTPs supplementation enhanced bacterial levels of Akkermansia and reduced levels of Ruminiclostridium_9. A significant reduction of glycolysis metabolism related to obesity and gut microbiota dysbiosis was also observed upon administration of DOTPs. Our results suggest that DOTPs can produce significant anti-obesity effects, by inhibiting systematic inflammation and ameliorating gut microbiota dysbiosis in diet-induced obese mice.

Development and validation of competitive risk model for older women with metaplastic breast cancer.

BACKGROUND: Metaplastic breast cancer (MpBC) is a rare histological subtype of breast cancer. This study aims to establish a competitive risk model for older women with MpBC to predict patients' survival accurately. METHODS: Data on patients diagnosed with MpBC from 2010 to 2019 are from the Surveillance, Epidemiology and End Results (SEER) program in the United States. All patients were randomly assigned to the training set and validation set. The proportional sub-distribution risk model was used in the training set to analyze the risk factors affecting patient death. Based on the risk factors for cancer-specific mortality (CSM) in patients, we constructed a competitive risk model to predict patients' 1-, 3-, and 5-year cancer-specific survival. Then we used the concordance index (C-index), the calibration curve and the area under the receiver operating characteristic curve (AUC) to validate the discrimination and accuracy of the model. RESULTS: One thousand, four hundred twelve older women with MpBC were included in this study. Age, T stage, N stage, M stage, tumor size, surgery and radiotherapy were risk factors for CSM. We established a competitive risk model to predict 1-, 3-, and 5-year cancer-specific survival in older women with MpBC. The C-index of the model was 0.792 in the training set and 0.744 in the validation set. The calibration curves in the training and validation sets showed that the model's predicted values were almost consistent with the actual observed values. The AUC results show that the prediction model has good accuracy. CONCLUSION: We developed a competitive risk model based on these risk factors to predict cancer-specific survival in older women with MpBC. The validation results of the model show that it is a very effective and reliable prediction tool. This predictive tool allows doctors and patients to make individualized clinical decisions.

A pan-cancer analysis of ring finger protein 135 and its relationship to triple-negative breast cancer proliferation and metastasis.

Ring finger protein 135 (RNF135) is an E3 ubiquitin ligase with RING finger domains that plays a crucial role in the development of several forms of cancer. Neither the expression profile of RNF135 nor its importance in the diagnosis of pan-cancer have been elucidated as of yet. With the aid of The Cancer Genome Atlas and Gene Expression Omnibus, we have fully mapped the expression profiles, prognostic relevance, genetic modification, immune cell infiltration, and tumor heterogeneity of RNF135 in 33 malignant tumors. RNF135 was expressed inconsistently in various cancers, and variations in RNF135 expression predicted survival outcomes for cancer patients. There was a strong correlation between the levels of the RNF135 genetic mutation and some tumor progression. In addition, a strong correlation was seen between RNF135 expression and immune cell infiltration, tumor mutation burden, microsatellite instability, and immunoregulators. In contrast, the correlation between RNF135 expression and triple-negative breast cancer was investigated in this study. RNF135 may boost the proliferation, migration, and invasion of TNBC cells, according to cell experiments. RNF135 might be utilized as a biomarker to anticipate how a tumor will behave and may have a significant role in how TNBC cells grow and migrate, according to the findings of this study.

A multicentre single arm phase 2 trial of neoadjuvant pyrotinib and letrozole plus dalpiciclib for triple-positive breast cancer.

Current therapies for HER2-positive breast cancer have limited efficacy in patients with triple-positive breast cancer (TPBC). We conduct a multi-center single-arm phase 2 trial to test the efficacy and safety of an oral neoadjuvant therapy with pyrotinib, letrozole and dalpiciclib (a CDK4/6 inhibitor) in patients with treatment-naïve, stage II-III TPBC with a Karnofsky score of ≥70 (NCT04486911). The primary endpoint is the proportion of patients with pathological complete response (pCR) in the breast and axilla. The secondary endpoints include residual cancer burden (RCB)-0 or RCB-I, objective response rate (ORR), breast pCR (bpCR), safety and changes in molecular targets (Ki67) from baseline to surgery. Following 5 cycles of 4-week treatment, the results meet the primary endpoint with a pCR rate of 30.4% (24 of 79; 95% confidence interval (CI), 21.3-41.3). RCB-0/I is 55.7% (95% CI, 44.7-66.1). ORR is 87.4%, (95% CI, 78.1-93.2) and bpCR is 35.4% (95% CI, 25.8-46.5). The mean Ki67 expression reduces from 40.4% at baseline to 17.9% (P < 0.001) at time of surgery. The most frequent grade 3 or 4 adverse events are neutropenia, leukopenia, and diarrhoea. There is no serious adverse event- or treatment-related death. This fully oral, chemotherapy-free, triplet combined therapy has the potential to be an alternative neoadjuvant regimen for patients with TPBC.

A Novel Combined Nomogram Model for Predicting the Pathological Complete Response to Neoadjuvant Chemotherapy in Invasive Breast Carcinoma of No Specific Type: Real-World Study.

Objective: To explore the value of a predictive model combining the multiparametric magnetic resonance imaging (mpMRI) radiomics score (RAD-score), clinicopathologic features, and morphologic features for the pathological complete response (pCR) to neoadjuvant chemotherapy (NAC) in invasive breast carcinoma of no specific type (IBC-NST). Methods: We enrolled, retrospectively and consecutively, 206 women with IBC-NST who underwent surgery after NAC and obtained pathological results from August 2018 to October 2021. Four RAD-scores were constructed for predicting the pCR based on fat-suppression T2-weighted imaging (FS-T2WI), diffusion-weighted imaging (DWI), contrast-enhanced T1-weighted imaging (T1WI+C) and their combination, which was called mpMRI. The best RAD-score was combined with clinicopathologic and morphologic features to establish a nomogram model through binary logistic regression. The predictive performance of the nomogram was evaluated using the area under receiver operator characteristic (ROC) curve (AUC) and calibration curve. The clinical net benefit of the model was evaluated using decision curve analysis (DCA). Results: The mpMRI RAD-score had the highest diagnostic performance, with AUC of 0.848 among the four RAD-scores. T stage, human epidermal growth factor receptor-2 (HER2) status, RAD-score, and roundness were independent factors for predicting the pCR (P < 0.05 for all). The combined nomogram model based on these factors achieved AUCs of 0.930 and 0.895 in the training cohort and validation cohort, respectively, higher than other models (P < 0.05 for all). The calibration curve showed that the predicted probabilities of the nomogram were in good agreement with the actual probabilities, and DCA indicated that it provided more net benefit than the treat-none or treat-all scheme by decision curve analysis in both training and validation datasets. Conclusion: The combined nomogram model based on the mpMRI RAD-score combined with clinicopathologic and morphologic features may improve the predictive performance for the pCR of NAC in patients with IBC-NST.

Pyrotinib-Containing Neoadjuvant Therapy in Patients With HER2-Positive Breast Cancer: A Multicenter Retrospective Analysis.

Background: Pyrotinib, a small-molecule tyrosine kinase inhibitor, has been investigated as a component of neoadjuvant therapy in phase 2 trials of human epidermal growth factor receptor 2 (HER2)-positive breast cancer. This study aimed to evaluate the effectiveness and safety of pyrotinib-containing neoadjuvant therapy for patients with HER2-positive early or locally advanced breast cancer in the real-world setting. Methods: Data of 97 patients with HER2-positive breast cancer from 21 centers across China treated with pyrotinib-containing neoadjuvant therapy were reviewed. Neoadjuvant therapy consisted of taxane/carboplatin/trastuzumab plus pyrotinib (TCbH+Py, 30 [30.9%]), anthracycline/cyclophosphamide followed by taxane/trastuzumab plus pyrotinib (AC-TH+Py) or taxane followed by anthracycline/cyclophosphamide/trastuzumab plus pyrotinib (T-ACH+Py, 29 [29.9%]), taxane/trastuzumab plus pyrotinib (TH+Py, 23 [23.7%]), and other pyrotinib-containing neoadjuvant treatment (15 [15.5%]). The primary outcome was breast pathological complete response (bpCR, ypT0/is) rate. Secondary outcomes included total pathological complete response (tpCR, ypT0/is ypN0) rate, objective response rate (ORR), and the incidence of preoperative adverse events. Results: The ORR of pyrotinib-containing neoadjuvant therapy was 87.6% (85/97). The bpCR and tpCR rates were 54.6% (95% confidence interval [CI], 44.2%-64.7%) and 48.5% [95% CI, 38.2%-58.8%], respectively. The most common grade 3 or 4 treatment-related adverse events included diarrhea (15 [15.5%]), decreased hemoglobin (nine [9.3%]), and decreased neutrophil count (eight [8.2%]). No treatment-related deaths occurred. Conclusion: Pyrotinib-containing neoadjuvant therapy for patients with HER2-positive early or locally advanced breast cancer shows favorable effectiveness with manageable toxicity in the real-world setting. Trastuzumab plus pyrotinib may be a novel option of dual HER2-targeted blockade.

Aromatase inhibitors plus ovarian function suppression versus tamoxifen plus ovarian function suppression for premenopausal women with early stage breast cancer: a systematic review and meta-analysis.

In the NCCN guidelines version 1.2019, aromatase inhibitors (AIs) or tamoxifen (TAM) for 5 years plus ovarian function suppression (OFS) were recommended for premenopausal breast cancer patient who has higher risk of recurrence. The meta-analysis established a comparison of the curative effect of two adjuvant endocrine therapies. In order to obtain randomized controlled trials (RCTs) related to this metaanalysis, PubMed and Embase database were searched systematically in English during May 2019. Two reviewers screened the articles and extracted data based on the criteria recommended by the Cochrane collaboration for evaluating evidence in RCTs. The first outcome was disease-free survival (DFS). Overall survival (OS) was the other endpoint. Hazard ratios (HRs) with 95% confidence intervals (CIs) were pooled utilizing fixed-effect model. The heterogeneity of this study has been described by Cochran's Q and the I2 statistics. Three RCTs which involved 7,203 premenopausal women with breast cancer were available in this meta-analysis. Pooled HRs showed that there was not difference between AIs plus OFS and TAM plus OFS in DFS (HR =0.87, 95% CI: 0.66-1.14, P=0.30). No statistical differences were found in OS between the two adjuvant therapies (HR =1.22, 95% CI: 0.75-1.99, P=0.43). Based on the included studies, there were no statistical differences between AIs plus OFS and TAM plus OFS in DFS and OS.

miR-211 alleviates ischaemia/reperfusion-induced kidney injury by targeting TGFßR2/TGF-ß/SMAD3 pathway.

MicroRNA-211 (miR-211) is closely related to apoptosis and plays an important role in ischemia/reperfusion (I/R) injury. Whether miR-211 is involved in the protective effects in renal I/R injury is unknown. In this study, we evaluated the role of miR-211 in human tubular epithelial cells in response to hypoxia-reoxygenation (H/R) stimulation and I/R injury in vitro and in vivo. The results revealed that miR-211 was down-regulated and TGFßR2 was up-regulated in human kidney (HK-2) cells subjected to H/R. Luciferase reporter assay showed that TGFßR2 was a direct target of miR-211. Enforced miR-211 expression decreased H/R-induced HK-2 cell apoptosis and increased cell viability, and targeting miR-211 further increased H/R-induced HK-2 cell apoptosis and decreased cell viability. However, the effect of miR-211 was reversed by targeting TGFßR2 or enforced TGFßR2 expression in miR-211 overexpressing cells or miR-211 downexpressing cells. Moreover, we confirmed that miR-211 interacted with TGFßR2, and regulating TGF-ß/SMAD3 signal. In vivo in mice, miR-211 overexpression ameliorates biochemical and histological kidney injury, reduces apoptosis in mice following I/R. On the contrary, miR-211 downexpressing promoted histological kidney injury and increased apoptosis in mice following I/R. Inhibition of miR-211 or miR-211 overexpression inhibited TGF-ß/SMAD3 pathways or activated TGF-ß/SMAD3 signal pathways in vitro and in vivo, which are critical for cell survival. Our findings suggested that miR-211 suppress apoptosis and relieve kidney injury following H/R or I/R via targeting TGFßR2/TGF-ß/SMAD3 signals. Therefore, miR-211 may be as therapeutic potential for I/R- induced kidney injury.

Preparation and Property of Perfluoropolyether Emulsions.

Perfluoropolyether (PFPE) glycerol emulsions were prepared. Three different green surfactants (AES (sodium laureth sulfate), APG (alkyl polyglycoside), and SDS (sodium dodecyl sulfate)) were chosen to emulsify the PFPE. Their properties and performance in shampoo were also investigated. Centrifuge stability measurements show that three PFPE emulsions have good stability. They are stable for 60 min when the centrifugal speed is 6000 r/min. In addition, a change of droplet size was observed with time. Moreover, its rheological properties and application performance was studied. The AES emulsion was the most stable emulsion and it was found to improve the slip and lubricity performance of the cotton, so it has potential applications in shampoo.

Serum miR-22 Could be a Potential Biomarker for the Prognosis of Breast Cancer.

BACKGROUND: This study aims to evaluate whether miR-22 could be used as a potential biomarker to screen breast cancer patients from healthy controls. This has never been explored. METHODS: Real time PCR analysis was carried out to explore the expression of serum miR-22 in breast cancer patients. Chi-square test was used for counting data. Log rank test was used for comparing survival curves. CoX regression model was used for univariate and multivariate prognosis analysis. In addition, we also evaluated the role of miR-22 on the migration capacity of MCF-7 cells using a wound healing assay. RESULTS: We found that low expression of miR-22 was significantly associated with late TNM stage, lymph node metastasis, local recurrence, and distant metastasis. Meanwhile, low expression of miR-22 was significantly associated with short survival and poor prognosis in all patients and lymph node subgroups. Analysis of CoX univariate and multivariate models demonstrated that miR-22 is an independent prognostic marker of breast cancer. In ad-dition, overexpression of miR-22 significantly decreased the migration of MCF-7 cells, validating the tumor suppressor role of miR-22 in breast cancer cells. CONCLUSIONS: In summary, low miR-22 expression may be a potential biomarker to screen breast cancer patients from healthy control.

Targeting MIAT reduces apoptosis of cardiomyocytes after ischemia/reperfusion injury.

This study aims to investigate the role of targeting lncRNA myocardial infarction-associated transcript (MIAT) in protection against hypoxia/reoxygenation (H/R) injury in H9c2 cells in vitro and myocardial ischemia/reperfusion (I/R) injury in vivo by regulating expression of NF-kB and p53 upregulated modulator of apoptosis (PUMA). H9C2 cells were infected with lentivirus expressing the short-hairpin RNA direct against human MIAT gene (Lv-MIAT shRNA) or lentivirus expressing scrambled control (Lv-NC shRNA) or PUMA siRNA or p65 siRNA or their control siRNA respectively. Then the H9c2 cells were infected with Lv-shRNA to 2 hours of hypoxia (H) and 24 hour of reoxygenation (R). 100 ul of Lv-MIAT shRNA (1 × 108 PFU) or Lv-NC shRNA was transfected into mouse hearts, then the hearts were subjected to I/R (1h/72 h). We discovered targeting MIAT remarkably enhanced H9c2 cell viability, decreased H/R-induced cell apoptosis and LDH leakage and significantly decreased I/R-induced myocardial infarct size, reduced myocardial apoptosis and enhanced the heart function. Targeting MIAT downregulated p65 nuclear translocation, NF-κB activity and anti-apoptotic protein cleaved-caspase-3, Bax, and upregulated anti-apoptotic protein Bcl-2 induced by H/R or I/R. Our study suggests that targeting MIAT may protect against H9c2 cardiomyoblasts H/R injury or myocardial I/R injury via inhibition of cell apoptosis, mediated by NF-κB and PUMA signal pathway.

The Contrary Effects of Sirt1 on MCF7 Cells Depend on CD36 Expression Level.

BACKGROUND: Breast cancer is one of the most aggressive and pervasive cancers identified in females. Sirt1 and CD36 both exert an essential role toward the oncogenic signaling in breast cancer cells. As reported, the adrenergic signaling could promote the malignancy of breast cancer. This study focuses specifically on the role of Sirt1/CD36 in the proliferation of MCF-7 breast cancer cells and also investigates their response to the α2-adrenergic agonist dexmedetomidine (Dex). MATERIALS AND METHODS: Expression of Sirt1 and CD36 was measured in breast cancer tissue by immunohistochemistry. We cultured MCF7 cells and treated cells with resveratrol (RSV) or Dex. Western blot analysis was performed to quantify the protein expression levels. The methyl thiazolyl tetrazolium (MTT) assay was applied to detect cell proliferation. RESULTS: Compared with normal adjacent tissues, Sirt1 increased and CD36 decreased in cancer tissues. RSV, a Sirt1 activator, increased the proliferation of MCF-7 cells at low concentration but exerted cytotoxicity effect at higher concentration. Sirt1 activation increased the expression of CD36 at higher concentration. Dex treatment gradually increased the proliferation of MCF7 cells in a dose-dependent manner and downregulated the expression of Sirt1/CD36. Interestingly, overexpression of Sirt1 via RSV pretreatment could suppress Dex-stimulated proliferation of breast cancer, accompanied with CD36 upregulation. CONCLUSIONS: though expression of Sirt1 increased in breast cancer progression, overexpression of Sirt1 could inhibit MCF7 proliferation, which may be associated with CD36 upregulation. In addition, the promotion effect of Dex on MCF7 cells, which may be associated with the Sirt1/CD36 inhibition, could be weakened by Sirt1 activation via RSV.

A study on the biological function of heat shock factor 1 proteins in breast cancer.

The present study aimed to investigate the effect of HSF1 proteins on cell proliferation, apoptosis and invasion of breast cancer. The Michigan Cancer Foundation-7 (MCF-7) HSF1-knocked down stable cell line (experimental group) and control cell line (control group) were obtained using a lentivirus assay, and the effects of HSF1 knockdown on the proliferation, tumor formation, apoptosis and invasion ability were analyzed, respectively. The effects of HSF1 on downstream signals were analyzed using western blotting. Western blotting results showed that lentivirus successfully established a HSF1 knockdown stable cell line of MCF-7. Compared with the control group, the growth rate of MCF-7 cells in the experimental group was significantly decreased (P<0.05). Flow cytometry showed that the proportion of apoptosis in the control group was significantly lower than that of the experimental group (P<0.05). Notably, the invasion ability of cells in the control group was significantly higher than that in the experimental group (P<0.05). Compared with cells in the control group, the levels of heat shock protein (HSP)70, HSP90, anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and macrophage migration inhibitory factor (MIF) in the experimental group were significantly downregulated, whereas the level of Bax was significantly increased (P<0.05). In conclusion, HSF1 protein, as a transcription factor, regulates the expression levels of HSP70, HSP90, MIF, Bcl-2 and Bax, thus controlling the proliferation, apoptosis and invasion of cells. These findings suggest HSF1 protein as a potential target for the treatment of breast cancer.