Erratum: Curcumin induces apoptosis in breast cancer cells and inhibits tumor growth and .

[This corrects the article on p. 2818 in vol. 7, PMID: 25031701.

Erratum: CXCL12 chemokine expression suppresses human breast cancer growth and metastasis in vitro and in vivo.

[This corrects the article on p. 6671 in vol. 7, PMID: 25400746.

Erratum: [Corrigendum] Mesenchymal stem cells expressing interleukin‑18 suppress breast cancer cells .

[This corrects the article DOI: 10.3892/etm.2015.

Erratum: [Corrigendum] Mesenchymal stem cells expressing interleukin‑18 inhibit breast cancer in a mouse model.

[This corrects the article DOI: 10.3892/ol.2018.

[Retracted] TGF‑β1 induces peritoneal fibrosis by activating the Smad2 pathway in mesothelial cells and promotes peritoneal carcinomatosis.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the fluorescence microscopy data shown in Fig. 6A and B were strikingly similar to data appearing in different form in Fig. 7 in a previously published paper [Lv Z‑D, Na D, Liu F‑N, Du Z‑M, Sun Z, Li Z, Ma X‑Y, Wang Z‑N and Xu H‑M: Induction of gastric cancer cell adhesion through transforming growth factor‑beta1‑mediated peritoneal fibrosis.

Paired‑related homeobox 1 overexpression promotes multidrug resistance via PTEN/PI3K/AKT signaling in MCF‑7 breast cancer cells.

Multidrug resistance (MDR) is a major cause of disease relapse and mortality in breast cancer. Paired‑related homeobox 1 (PRRX1) is associated with the epithelial‑mesenchymal transition (EMT), which is involved in tumor development, including cell invasion and MDR. However, the effect of PRRX1 on MDR had not clearly established.

A randomized multicenter phase II trial of mecapegfilgrastim single administration versus granulocyte colony-stimulating growth factor on treating chemotherapy-induced neutropenia in breast cancer patients.

Background: This study aimed to evaluate the efficacy and safety of mecapegfilgrastim (HHPG-19K) with different doses compared to granulocyte colony-stimulating growth factor (G-CSF) in treating chemotherapy-induced neutropenia in breast cancer patients.

Methods: A total of 182 breast cancer patients were enrolled in this multi-center, randomized, phase II trial and developed neutropenia after first cycle chemotherapy. Patients were then assigned as 1:1:1 ratio to receive 100 µg/kg HHPG-19K single injection (HHPG-19K-N group), 150 µg/kg HHPG-19Ksingle injection (HHPG-19K-H group) and 5 µg/kg G-CSF daily injection (G-CSF group) at day 3 of the second cycle (cycle 2) chemotherapy.

p53-independent role of MYC mutant T58A in the proliferation and apoptosis of breast cancer cells.

Myc proto-oncogene (MYC) is an oncoprotein that promotes proliferation and apoptosis. MYC mutations frequently disrupt the apoptotic processes during tumorigenesis. In the present study, the effects of the MYC point mutation T58A on the progression of a cellular tumor antigen p53 (p53) human breast cancer cell line was analyzed, and the mechanism of p53-independent MYC-induced apoptosis was investigated.

miR-135b promotes proliferation and metastasis by targeting APC in triple-negative breast cancer.

Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype. The aim of our study was to investigate the functional role of microRNA-135b (miR-135b) in TNBC. A real-time polymerase chain reaction assay was used to quantify miR-135b expression levels in 90 paired TNBC tissue and adjacent normal tissue samples.

Mesenchymal stem cells expressing interleukin-18 inhibit breast cancer in a mouse model.

Development of an improved breast cancer therapy has been an elusive goal of cancer gene therapy for a long period of time. Human mesenchymal stem cells derived from umbilical cord (hUMSCs) genetically modified with the interleukin (IL)-18 gene (hUMSCs/IL-18) were previously demonstrated to be able to suppress the proliferation, migration and invasion of breast cancer cells . In the present study, the effect of hUMSCs/IL-18 on breast cancer in a mouse model was investigated.

PRRX1 drives tamoxifen therapy resistance through induction of epithelial-mesenchymal transition in MCF-7 breast cancer cells.

Purpose: Resistance to endocrine therapies is a major cause of disease relapse and mortality in estrogen receptor (ER)-positive breast cancers, which has been associated with tumor epithelial-mesenchymal transition (EMT). In this study, we investigated the contribution of the EMT-inducing factor paired related homeobox 1 (PRRX1) to tamoxifen (TAM) resistance acquired using ER-positive MCF-7 breast cancer cells.

Methods: PRRX1 was overexpressed in MCF-7 cells through transfection; cells transfected with a blank vector served as the control.

Silencing of Prrx2 Inhibits the Invasion and Metastasis of Breast Cancer both In Vitro and In Vivo by Reversing Epithelial-Mesenchymal Transition.

Background/aims: Epithelial-mesenchymal transition (EMT) is recognized as a crucial mechanism in breast cancer progression and metastasis. Paired-related homeobox 2 (Prrx2) has been identified as a new EMT inducer in cancer, but the underlying mechanisms are still poorly understood.

Methods: The expression of Prrx2 was assessed by immunohistochemistry in breast cancer tissues to evaluate the clinicopathological significance of Prrx2, as well as the correlation between Prrx2 and EMT.

Silencing of Prrx1b suppresses cellular proliferation, migration, invasion and epithelial-mesenchymal transition in triple-negative breast cancer.

Triple-negative breast cancer (TNBC) is a highly aggressive tumour subtype associated with poor prognosis. The mechanisms involved in TNBC progression remains largely unknown. To date, there are no effective therapeutic targets for this tumour subtype.

miR-655 suppresses epithelial-to-mesenchymal transition by targeting Prrx1 in triple-negative breast cancer.

Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer subtype that lacks effective targeted therapies. The epithelial-to-mesenchymal transition (EMT) is a key contributor in the metastatic process. In this study, we found that miR-655 was down-regulated in TNBC, and its expression levels were associated with molecular-based classification and lymph node metastasis in breast cancer.

[Effect of miRNA-135b on proliferation, invasion and migration of triple-negative breast cancer by targeting APC].

Objective: To explore the expression of miRNA-135b in a variety of breast cancer cell lines and its function on the proliferation, invasion and migration in triple-negative breast cancer cell lines by targeting adenomatous polyposis coli (APC).

Methods: Quantitative real-time (RT)--PCR was used to detect the expression of miRNA-135b in seven breast cancer cell lines and one normal breast cell line. The three-negative breast cancer cell lines MDA-MB-231 and MDA-MB-468 with miRNA-135b high-expression were divided into three groups: the normal growth group, the negative control group (transfected with negative counter-part) and the experimental group (transfected with miRNA-135b inhibitors).

NKD1 down-regulation is associated with poor prognosis in breast invasive ductal carcinoma.

As a negative modulator of the canonical Wnt signaling pathway, Naked1 (NKD1) is widely expressed in many normal tissues. However, the expression and clinicopathological significance of NKD1 in patients with breast cancer is still unclear. The aim of this study was to evaluate NKD1 expression in breast cancer and to investigate the question of whether reduced expression of NKD1 may have any pathological significance in breast cancer development or progression.

Mesenchymal stem cells expressing interleukin-18 suppress breast cancer cells .

Breast cancer is the most common malignancy among females throughout the world. Current treatments have unsatisfactory outcomes due to the dispersed nature of certain types of the disease. The development of a more effective therapy for breast cancer has long been one of the most elusive goals of cancer gene therapy.

[Role of transforming growth factor-β1 in epithelial-mesenchymal transition of mesothelial cells and its effect on peritoneal metastasis of gastric cancer].

Objective: To elucidate the role of transforming growth factor-beta1(TGF-β1) in epithelial-mesenchymal transition of mesothelial cells and peritoneal metastasis of gastric cancer.

Methods: HMrSV5 cells, a human peritoneal mesothelial cell line, were incubated with TGF-β1, and their morphological changes were observed by phase contrast microscopy. Expressions of α-smooth muscle actin (α-SMA), vimentin, cytokeratin, E-cadherin, phosphorylated-Smad2 and Smad2 were examined by Western blotting.

CXCL12 chemokine expression suppresses human breast cancer growth and metastasis in vitro and in vivo.

Chemokine receptors are now known to play an important role in cancer growth and metastasis. However, there is little information regarding chemokine expression in breast cancer. The aim of this study was to evaluate CXCL12 expression in breast cancer and to investigate the question of whether reduced expression of CXCL12 may have any pathological significance in breast cancer development or progression.

[Effect of interleukin-18 gene modified human umbilical cord mesenchymal stem cells on proliferation of breast cancer cell].

Objective: To establish human umbilical cord mesenchymal stem cells (HUMSCs) strain transfected with interleukin-18 (IL-18) gene and examine its effects on the proliferation of breast cancer cell (MCF-7).

Methods: HUMSCs were isolated and cultured. And the lentivirus-IL-18 vector containing human IL-18 gene was constructed and transfected into HUMSCs.

Curcumin induces apoptosis in breast cancer cells and inhibits tumor growth in vitro and in vivo.

Curcumin has shown therapeutic and/or adjuvant therapeutic effects on the treatment of some patients with breast cancer. However, its mechanisms of action are largely unknown. This study was designed to investigate its antitumor effect and underlying mechanisms in human breast cancer MDA-MB-231 and MCF-7 cells.

[Anti-apoptotic mechanism for p21(waf1) in human basal like breast cancer cell line HCC1937].

Objective: To explore the anti-apoptotic mechanism of p21(waf1) in human basal like breast cancer cell line HCC1937.

Methods: There were 3 groups, i.e.

Effects of two different immunotherapies on triple negative breast cancer in animal model.

The ability of immune system to react specifically against tumors inspirited the study of triple negative breast cancer (TNBC) immunotherapies. Sixty spontaneous breast cancer TA2 mice were randomly divided into three groups: GM-CSF group, with therapy of granulocyte-macrophage colony-stimulating factor (GM-CSF) combined with breast cancer stem cells associated antigens and cytosine-phosphorothioate-guanine oligodeoxynucleotides (CpG-ODNs); DC-CIK group, with infusions of dendritic cells/cytokine-induced killer (DC/CIK) cells; and PBS group as controls. After therapy, the cellular immunity of mice in GM-CSF group and DC-CIK group was obviously increased, especially for GM-CSF group (P<0.

Efficacy of combined therapy of goserelin and letrozole on very young women with advanced breast cancer as first-line endocrine therapy.

Breast cancer in young women younger than 35 years old is rare, aggressive and associated with a poor prognosis. Endocrine therapy is a preferred treatment modality in hormone receptor-positive early stage and advanced breast cancer, combined therapy of goserelin and letrozole presents an option for premenopausal women. We reported the efficacy and safety of therapy of goserelin plus letrozole on very young women with advanced breast cancer as first-line endocrine therapy.