Expression of proliferation and apoptosis-related proteins in usual ductal hyperplasia of the breast

1998 ◽  
Vol 29 (12) ◽  
pp. 1539-1545 ◽  
Author(s):  
Ellen C.M Mommers ◽  
Paul J Van Diest ◽  
Angelique M Leonhart ◽  
Chris J.L.M Meijer ◽  
Jan P.A Baak
2022 ◽  
Vol 12 (2) ◽  
pp. 306-315
Author(s):  
Jie Song ◽  
Cheng Chen ◽  
Hui Zhang

Osteoarthritis (OA) is a chronic and inflammatory disease, leading to pain or even disability in severe cases. LncRNA PCGEM1 (PCGEM1) is reported to be dysregulated, serving as critical regulators in various human diseases, including OA. However, the biological role of PCGEM1 and its underlying mechanisms during OA remained unclear. In the present study, CHON-001 cells were exposed to interleukin (IL)-1β to construct the OA cell model. Expression of PCGEM1 and miR-152-3p in cells was determined by quantitative real-time polymerase chain reaction (qRT-PCR) assay. Corresponding commercial kits were used to measure the expressions of lactate dehydrogenase (LDH), inter-leukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α. Protein levels of apoptosis-related proteins, cleaved-Caspase3 and Caspase3, were detected by Western blotting. 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide) tetrazolium (MTT) and flow cytometry assays were utilized for the determination of cell proliferation and apoptosis. The association between PCGEN1 and miR-152-3p was confirmed by a dual-luciferase reporter assay. From the results, PCGEM1 expression was significantly increased while miR-152-3p was inhibited in CHON-001 cells after IL-1β treatment. In addition, silencing of PCGEM1 could promote proliferation, inhibit the apoptosis, suppress LDH level and alleviate inflammation response caused by IL-1β in CHON-001 cells by sponging miR-152-3p. In a word, PCGEM1 down-regulation suppressed OA progression by the regulation of miR-152-3p expression, functioning as a potential therapeutic target for OA clinical treatment.


2018 ◽  
Vol 6 ◽  
pp. 205031211881154 ◽  
Author(s):  
Ichiro Maeda ◽  
Shinya Tajima ◽  
Yoshihide Kanemaki ◽  
Koichiro Tsugawa ◽  
Masayuki Takagi

Objectives: The aim of this study was to use immunohistochemistry to differentiate solid papillary carcinoma in situ from intraductal papilloma with usual ductal hyperplasia (IPUDH). Three types of high-molecular-weight cytokeratins (CKs) – CK5/6, CK14, and CK34betaE12 – were targeted. Methods: We studied 17 patients with solid papillary carcinoma in situ and 18 patients with IPUDH diagnosed by at least two pathologists. Immunohistochemical analyses used antibodies to CK5/6, CK14, and CK34betaE12 to make the differential diagnosis of solid papillary carcinoma in situ versus IPUDH. Immunohistochemical staining was scored as 0–5 using Allred score. Results: Immunohistochemistry with CK5/6 and CK14 antibodies produced scores of 0–3 in all patients with solid papillary carcinoma in situ and 2–5 in all patients with IPUDH. Immunohistochemical staining with CK34betaE12 antibody produced scores of 1–3 in all patients with solid papillary carcinoma and 3–5 in all patients with IPUDH. In tissues from patients with IPUDH, significantly more cells were stained with CK34betaE12 than CK5/6 ( p < 0.05) or CK14 ( p < 0.05). Conclusion: The immunoreactivity of CK5/6, CK14, and CK34betaE12 antibodies was useful to differentiate solid papillary carcinoma in situ from IPUDH. CK34betaE12 is especially useful for distinguishing solid papillary carcinoma from IPUDH.


2021 ◽  
Vol 12 ◽  
Author(s):  
Qin Zhang ◽  
Jing Long ◽  
Nannan Li ◽  
Xuelian Ma ◽  
Lisheng Zheng

Hyperglycemia exposure results in the dysfunction of endothelial cells (ECs) and the development of diabetic complications. Circular RNAs (circRNAs) have been demonstrated to play critical roles in EC dysfunction. The current study aimed to explore the role and mechanism of circRNA CLIP–associating protein 2 (circ_CLASP2, hsa_circ_0064772) on HG-induced dysfunction in human umbilical vein endothelial cells (HUVECs). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess the levels of circ_CLASP2, miR-140-5p and F-box, and WD repeat domain-containing 7 (FBXW7). The stability of circ_CLASP2 was identified by the actinomycin D and ribonuclease (RNase) R assays. Cell colony formation, proliferation, and apoptosis were measured by a standard colony formation assay, colorimetric 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazolium bromide (MTT) assay, and flow cytometry, respectively. Western blot analysis was performed to determine the expression of related proteins. Targeted correlations among circ_CLASP2, miR-140-5p, and FBXW7 were confirmed by dual-luciferase reporter assay. High glucose (HG) exposure downregulated the expression of circ_CLASP2 in HUVECs. Circ_CLASP2 overexpression or miR-140-5p knockdown promoted proliferation and inhibited apoptosis of HUVECs under HG conditions. Circ_CLASP2 directly interacted with miR-140-5p via pairing to miR-140-5p. The regulation of circ_CLASP2 overexpression on HG-induced HUVEC dysfunction was mediated by miR-140-5p. Moreover, FBXW7 was a direct target of miR-140-5p, and miR-140-5p regulated HG-induced HUVEC dysfunction via FBXW7. Furthermore, circ_CLASP2 mediated FBXW7 expression through sponging miR-140-5p. Our current study suggested that the overexpression of circ_CLASP2 protected HUVEC from HG-induced dysfunction at least partly through the regulation of the miR-140-5p/FBXW7 axis, highlighting a novel therapeutic approach for the treatment of diabetic-associated vascular injury.


2019 ◽  
Vol 3 (2) ◽  
pp. 41
Author(s):  
Kelvin Setiawan ◽  
Bramastha Aires Rosadi ◽  
Terry Renata Lawanto ◽  
Primariadewi Rustamadji

Background: Benign breast disease have been broadly classified into non-proliferative lesions, proliferative lesions without atypia and hyperplasia with atypia. Proliferative disease, such as usual ductal hyperplasia, is associated with a 1.5 to 2 fold increased risk of developing invasive carcinoma. We reported a case of usual ductal hyperplasia in a young male. Case: A 22-year-old male complained of discomfort and enlargement of unilateral breast. Physical examination at that time revealed a palpable mass in the lateral upper quadrant of the patient’s left breast, three centimeters from nipple areola complex. The examination of axilla didn’t reveal any lymph node enlargement on both sides. His vital signs were normal without any abnormalities found on examination. Ultrasonography examination demonstrated fibroglandular tissue in the left breast with the volume of 11.13 cm3, consist of 4.8 cm length, 2.9 cm width and 0.8 cm depth. Excisional tumor biopsy was done on his left breast. Usual duct cell hyperplasia was present in microscopic examination with chronic inflammatory cells spreading around the fibrotic stromal cell. Physical examination, radiologic examination, and biopsy were all performed in this patient. Although the accuracy of the triple test is high, benign concordant results do not obviate further surveillance of a palpable mass. We advised our patient to routinely follow-up his condition every 6 months for 1 to 2 years, especially if there any changes found on his breasts. Conclusion: Any guidelines and further studies regarding patient’s follow-up examination after biopsy for male breasts tumor are needed in order of better understanding about this disease.


2017 ◽  
Author(s):  
Richard J Bleicher

Clinicians who treat breast disease deal with a variety of pathologic findings. Although there is often a focus on paradigms and data regarding malignant breast disease, benign breast disease ranges from that which requires no imaging, evaluation, or treatment to that which requires further testing to rule out concomitant cancer and ameliorate subsequent risk. This review discusses the most frequent types of high-risk lesions facing the breast practitioner, including atypical ductal hyperplasia, lobular neoplasia, radial scar, and papillary lesions. It is critical that the clinician understand the implications of each finding to advise about the risks associated with each of these entities, fully assess the need for further therapy, and mitigate the patient’s future risk.  This review contains 2 tables, and 69 references. Key words: atypical ductal hyperplasia, atypical lobular hyperplasia, lobular neoplasia, lobular carcinoma in situ, papillary lesions, pleomorphic, pseudoangiomatous stromal hyperplasia, radial scar, usual ductal hyperplasia


2021 ◽  
Author(s):  
Daolu Zhan ◽  
Jian Liu ◽  
Mingxia Lin ◽  
Jian Chen ◽  
Yehan Fang ◽  
...  

Abstract The proliferation and apoptosis of nucleus pulposus (NP) cells (NPCs) play a crucial role in intervertebral disc degeneration (IDD). we aimed to discover the role of miRNA-induced IDD. We analyzed the miRNA expression of three NP tissues from IDD patients and three normal NP samples using the GEO2R tool, and The results revealed that miR-338-3p was upregulated in NPCs from IDD patients. miR-338-3p suppressed NPCs proliferation, and the related proteins PCNA and Ki-67 were downregulated, as demonstrated via western blotting. miR-338-3p promoted apoptosis. Furthermore, we predicted that HIF-1α was targeted by miR-338-3p, using the miRDB database, and this target was validated via dual luciferase assay. HIF-1α reversed miR-338-3p-induced NPCs proliferation and apoptosis. The Hippo-YAP pathway activation proteins YAP, CTGF, and PCNA were upregulated, unlike the inhibitory YAP phosphorylation. In conclusions, our results suggestive that miR-338-3p inhibited HIF-1α/ Hippo-YAP pathway to attenuate NPCs proliferation and apoptosis.


Author(s):  
Anna Sapino ◽  
Davide Balmativola ◽  
Maria Giulia Disanto ◽  
Caterina Marchiò

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