To explore the effect of circRHOT1 on breast cancer progression and the underlying mechanism. Significantly, our data revealed that the depletion of circRHOT1 was able to repress the proliferation and induce the apoptosis of breast cancer cells. CircRHOT1 knockdown could remarkably inhibit the invasion and migration in the breast cancer cells. Meanwhile, the depletion of circRHOT1 enhanced the erastin-induced inhibition effect on cell growth of breast cancer cells. The circRHOT1 knockdown notably increased the levels of reactive oxygen species (ROS), iron, and Fe
2+
in breast cancer cells. Mechanically, circRHOT1 was able to sponge microRNA-106a-5p (miR-106a-5p) and inhibited ferroptosis by down-regulating miR-106a-5p in breast cancer cells. Besides, miR-106a-5p induced ferroptosis by targeting signal transducer and activator of transcription 3 (STAT3) in the system. Moreover, the overexpression of STAT3 and miR-106a-5p inhibitor could reverse circRHOT1 knockdown-mediated breast cancer progression. Functionally, circRHOT1 promoted the tumor growth of breast cancer
in vivo
. In conclusion, we discovered that circRHOT1 contributed to malignant progression and attenuated ferroptosis in breast cancer by the miR-106a-5p/STAT3 axis. Our finding provides new insights into the mechanism by which circRHOT1 promotes the development of breast cancer. CircRHOT1 and miR-106a-5p may serve as potential targets for breast cancer therapy.
Death receptor-3 (DR3) plays controversial roles in cancer. Currently, DR3 is known to be a functional receptor of vascular endothelial growth inhibitor (VEGI). The role of DR3 in breast cancer remains unclear. The present study investigated DR3 expression in a clinical cohort of breast cancer patients and its role in breast cancer cells in vitro. The expression of DR3 was examined in a breast cancer cohort using quantitative PCR (Q-PCR) and immunohistochemistry (IHC) in comparison to the patients' data. In vitro function of DR3 was examined through the targeting of this molecule in MCF7 and MDA-MB-231 breast cancer cells using ribozyme transgene technology. Decreased DR3 expression was noted in breast cancer tissues compared to normal tissues and decreased expression of DR3 was generally associated with a poorer prognosis as well as a significantly shorter long-term survival (p=0.038). Targeting of DR3 in vitro in breast cancer cell lines resulted in impaired migratory rates compared to respective control cells. Collectively, these data suggest a complex role for DR3 in breast cancer development and progression.
ObjectiveThis study aimed to investigate the clinicopathological factors of the false negative rate (FNR) and accuracy of sentinel lymph node biopsy (SLNB) mapping with 1% methylene blue dye (MBD) alone, and to examine how to reduce the FNR in patients with breast cancer.MethodsA total of 365 patients with invasive breast carcinoma who received axillary lymph node dissection after SLNB were retrospectively analyzed. SLNB was performed with 2 to 5 mL of 1% MBD. We studied the clinicopathological factors that could affect the FNR of SLNB.ResultsThe identification rate of sentinel lymph nodes (SLNs) was 98.3% (359/365) and the FNR of SLNB was 10.4% (16/154). Multivariate analysis showed that the number of dissected SLNs and metastatic lymph nodes were independent predictive factors for the FNR of SLNB. The FNR in patients with 1, 2, 3, and ≥4 SLNs was 23.53%, 15.79%, 3.85%, and 1.79%, respectively.ConclusionsSLNB mapping with MBD alone in patients with breast cancer can produce favorable identification rates. The FNR of SLNB decreases as the number of SLNs rises. Because of side effects of searching for additional SLNs and the FNR, removal of three or four SLNs may be appropriate.
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