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Non-coding RNAs, including Inc-RNA and miRNA, have been reported to regulate gene expression and are associated with cancer progression. MicroRNA-561-3p (miR-561-3p), as a tumor suppressor, has been reported to play a role in preventing cancer cell progression, and MALAT1 (Lnc-RNA) have also been demonstrated to promote malignancy in various cancers, such as breast cancer (BC). In this study, we aimed to determine the correlation between miR-561-3p and MALAT1 and their roles in breast cancer progression. The expression of MALAT1, mir-561-3p, and topoisomerase alpha 2 (TOP2A) as a target of miR-561-3p was determined in BC clinical samples and cell lines via qRT-PCR. The binding site between MALAT1, miR-561-3p, and TOP2A was investigated by performing the dual luciferase reporter assay. MALAT1 was knocked down by siRNA, and cell proliferation, apoptotic assays, and cell cycle arrest were evaluated. MALAT1 and TOP2A were significantly upregulated, while mir-561-3p expression was downregulated in BC samples and cell lines. MALAT1 knockdown significantly increased miR-561-3p expression, which was meaningfully inverted by co-transfection with the miR 561-3p inhibitor. Furthermore, the knockdown of MALAT1 by siRNA inhibited proliferation, induced apoptosis, and arrested the cell cycle at the G1 phase in BC cells. Notably, the mechanistic investigation revealed that MALAT1 predominantly acted as a competing endogenous RNA in BC by regulating the miR-561-3p/TOP2A axis. Based on our results, MALAT1 upregulation in BC may function as a tumor promoter in BC via directly sponging miRNA 561-3p, and MALAT1 knockdown serves a vital antitumor role in BC cell progression through the miR-561-3p/TOP2A axis.

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Background. Breast cancer is one of the leading causes of death in women worldwide. This causes an increase in free radicals, resulting in oxidative stress. The aim of this study was to determine the effect of breast cancer on oxidative stress and its relationship with hematological indices. Methods. This case-control study included 43 women with breast cancer and 37 age-matched healthy controls. Oxidative stress and its correlation with hematological profiles over seven months were evaluated. Finally, the data were compared between the two groups using the t -test and Pearson’s test, and the results were analyzed using the SPSS 24 software. Results. The results revealed that patients with breast cancer had significantly increased hemoglobin (HB), hematocrit (HCT), mean corpuscular volume (MCV), and mean corpuscular hemoglobin (MCH) levels compared with healthy subjects ( p < 0.05 ). In addition, oxidative stress parameters, such as superoxide dismutase (SOD), catalase (CAT), total oxidant status (TOS), and total antioxidant capacity (TAC), were significantly elevated. Glutathione peroxidase (GPX) and malondialdehyde (MDA) were significantly lower in patients with breast cancer than in the control group ( p < 0.05 ). Statistical significance in hematological indices showed a positive or negative correlation with oxidative stress parameters. Conclusion. Women with breast cancer showed a deranged complete blood count (CBC) pattern compared to healthy individuals.

This study aimed to measure the received dose to the pelvic region of patients during breast intraoperative electron radiation therapy (IOERT). Furthermore, we compared the findings with those of external beam radiation therapy. Finally, secondary ovarian and uterus cancer risks following breast IOERT were estimated. In the current study, the received dose to the pelvic surface of 18 female patients during breast IOERT boosts were measured by thermoluminescent dosimeter (TLD-100) chips. All patients were treated with 12 Gy given in a single fraction. To estimate the dose to the ovary and uterus of the patients, conversion coefficients for depth from the surface dose were obtained in a Rando phantom. Given the received dose to the pelvic region of the patients, secondary ovarian and uterus cancer risks following breast IOERT were estimated. The received doses to the ovary and uterus surface of the patients were 0.260 ± 0.155 mGy to 31.460 ± 6.020 mGy and 0.485 ± 0.122 mGy to 22.387 ± 15.476 mGy, respectively. Corresponding intra-pelvic (ovary and uterus) regional doses were 0.012 ± 0.007 mGy to 1.479 ± 0.283 mGy and 0.027 ± 0.001 mGy to 1.164 ± 0.805 mGy, respectively. Findings demonstrated that the ratio of the received dose by the pelvic surface to the regional dose during breast IOERT was much less than external beam radiation therapy. The mean of the secondary cancer risks for the ovary in 8 and 10 MeV electron beam energies were 135.722 ± 117.331 × 10−6 and 69.958 ± 28.072 × 10−6, and for the uterus were 17.342 ± 10.583 × 10−6 and 2.971 ± 3.604 × 10−6, respectively. According to our findings, the use of breast IOERT in pregnant patients can be considered as a safe radiotherapeutic technique, because the received dose to the fetus was lower than 50 mGy. Furthermore, IOERT can efficiently reduce the unnecessary dose to the pelvic region and lowers the risk of secondary ovarian and uterus cancer following breast irradiation.