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Objective: To investigate damaging effects of clomifene citrate (CC) on endometrial stromal cells (hEndoSCs), and to study effects of spermidine on autophagy and inflammatory cytokine expression in damaged endometrial stromal cells. Methods: Groups were firstly divided into control group, spermidine group, clomiphene group (CC group), CC+Spermidine group. MTT assay was used to detect cell survival rate of hEndoSCs after co-incubation with different concentrations of CC or Spermidine for 24 h. Content of intracellular reactive oxygen species (ROS) and level of apoptosis in cells of the 4 groups were detected by flow cytometry technique. Western blot was used to detect expressions of autophagy pathway-related proteins ULK1, p-ULK1, LC-3 H, and apoptosis-related proteins Bax, Bcl-2, Cleaved-caspase 3. RT-qPCR was used to detect mRNA expressions of IL-6, IL-1β and TNF-α. Results: Compared with control group, CC group showed decreased cell survival, increased apoptosis rate, ROS content, Bax, Cleaved-caspase 3 expressions, decreased Bcl-2 expression, decreased levels of autophagy-related proteins p-ULK1 and LC-3 II/I, and elevated expressions of inflammatory factors IL-6, IL-1β and TNF-α mRNA (P<0.01). There was no significant changes viability of cells in spermidine group compared with control group (P>0.05). Compared with CC group, cell survival rate in CC+spermidine group was significantly increased, apoptosis rate, ROS content, Bax and Cleaved-caspase 3 expressions were decreased, Bcl-2 expression was increased, expressions of autophagy-related proteins p-ULK1 and LC-3 H/I were elevated, while expressions of inflammatory factors IL-6, IL-1β and TNF-α mRNA were decreased (P<0.01). Conclusion: CC can inhibit endometrial stromal cell proliferation, promote apoptosis, and increase the transcript levels of inflammatory factors IL-6, IL-1β and TNF-α. Spermidine can reduce intracellular ROS in clomiphene-injured endometrial stromal cells by activating cellular autophagy, increase cell survival, and inhibit the expressions of inflammatory factors IL-6, IL-1β and TNF-α. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the expression of KANKI in endometrial cancer and its effect on the proliferation and migration of endometrial cancer. Methods: (1) TCGA database was used to analyze the expression of KANK1 and its survival analysis in endometrial cancer. (2) Real-time quantitative polymerase chain reaction was used to verify the effect of transfection of KANKI plasmid. Ishikawa and ECC1 cells were used to investigate the effect of KANK1 on cell cycle and apoptosis of endometrial cancer cells. The expression of cell cycle-related proteins was detected by Western blot, and the cell cycle and apoptosis levels were detected by flow cytometry. (3) Cell invasion and metastasis ability were detected by transwell assay and wound healing assay. Results: TCGA database analysis showed that KANK1 was low expressed in endometrial cancer and correlated with good prognosis. Overexpression of KANK1 downregulated the protein levels of Cyclin D1 and Cyclin D2 and blocked the cell cycle in G1 phase. Flow cytometry showed that the apoptosis level of KANK1-overexpression group (Ishikawa: 22.7%; ECC1: 19.0%) was higher than that of the control group (Ishikawa: 18.1%; ECC1: 15.3%), and the difference was statistically significant. Transwell assay and wound healing assay showed that the invasion and metastasis ability of endometrial cancer cells overexpressing KANK1 was diminished. Conclusion: This study demonstrates that KANK1 plays an anti-tumor role in endometrial cancer. The high expression of KANK1 is positively related to the good prognosis of endometrial cancer. KANKI inhibits the proliferation of endometrial cancer by inhibiting cancer cell cycle progression and promoting tumor cell apoptosis. In addition, KANK1 inhibits the invasion and metastasis of endometrial cancer. [ABSTRACT FROM AUTHOR]

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the expression of cellular retinoic acid binding protein 2 (CRABP2) in endometrial adenocarcinoma tissues and cells and its effects on the proliferation and invasion of endometrial adenocarcinoma cells as well as its molecular mechanism. Methods: A total of 24 pairs of endometrioid adenocarcinoma tissues and matched normal endometrial tissues were collected from Hengshui People's Hospital from June 2020 to April 2021, and human endometrial adenocarcinoma cells (An3ca and KLE) were cultured in vitro. The expression of CRABP2 in human endometrioid adenocarcinoma tissues and normal endometrial tissues was analyzed by immunohistochemistry and WB. The knockdown efficiency of CRABP2 in An3ca and KLE cells was detected by WB method, and the proliferation and invasion ability of An3ca and KLE cells after CRABP2 knockdown was detected by EDU method and Transwell assay, the expressions of key proteins related to Wnt/β-catenin pathway (β-catenin, c-Myc, cyclin-D1, MMP7 and MMP9) in An3ca and KLE cells after CRABP2 knockdown were detected by WB. The effects of CRABP2 on the growth of xenograft tumor and the expression of Ki67 and β-catenin in xenograft tumor tissues were observed in nude mice tumorigenesis assay. Results: Compared with normal endometrial tissue, the expression of CRABP2 was up-regulated in human endometrioid adenocarcinoma tissue. Expression of CRABP2 in An3ca and KLE cells decreased after transfection of shRNA targeting CRABP2 (all P<0.01). The proliferation and invasion ability of An3ca and KLE cells were decreased after CRABP2 knockdown (all P<0.01) and the Wnt/β -catenin pathway was inhibited (P<0.01). The tumor formation experiment showed that the tumor volume of transplanted tumor in nude mice decreased significantly after CRABP2 knockdown (P<0.01). Conclusion: CRABP2 can promote the proliferation and invasion of endometrioid adenocarcinoma cells by regulating theWnt/β-catenin pathway [ABSTRACT FROM AUTHOR]

Endometrial cancer is the gynecological cancer with the highest incident rate in Taiwan. Compared with other types of gynecological cancers, women generally do not have sufficient information about, and thus pay less attention to, endometrial cancer. For endometrial cancer, early diagnosis is important to achieving a high rate of survival. However, endometrial cancer has negative effects due to insufficient information, leading to women having an unrealistic illness representation that influences their coping behaviors and disease outcomes. Leventhal's self-regulation model indicates that the illness representation of patients is based on received external information and past experiences, and that patients undergo the three stages of illness representation, coping, and appraisal when suffering from disease. In this article, the Leventhal self-regulation model was applied to better understand the correlation between illness representation, coping behaviors, and disease outcomes in patients with endometrial cancer at different disease phases. Clinical health providers may utilize this selfregulation model to help patients with endometrial cancer develop positive illness representation and adopt active coping strategies to realize a better adjustment. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Clinical Nursing in Practice is the property of Journal of Clinical Nursing in Practice (Editorial Board, Shanghai Jiao Tong University Press) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Imaging Science & Photochemistry is the property of Imaging Science & Photochemistry Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective .To analyze retrospectively the hysteroscopic and morphological characteristics of endometrial polypoid (EP) lesion in infertile patients, so as to improve the diagnostic coincidence rate of hysteroscopy and histopathology. Methods : Those infertile patients performed hysteroscopy were analyzed retrospectively from February 2005 through July 2014. Hysteroscopic characteristics were then compared with histopathologic characteristics in those patients with EP. Results : 17.4% (1 372/7 884) of infertile patients were diagnosed with EP lesion by hysteroscopy. The morphological manifestation of EP lesion under hysteroscopy were as follows: endometrial neoplasm (88.0%, 1 207/1 372), endometrial local uplift (6.7%, 92/1 372), and endometrial coarse and fragment (5.3%, 73/1 372). The three most prevalent diagnoses by histopathology were endometrial polyp (83.0%, 1 139/1 372), endometrial polypoid hyperplasia (9.3%, 128/1 372) and hysteromyoma (2.2%, 31/1 372). The diagnostic coincidence rate in those patients with typical polypoid neoplasm under hysteroscopy was significantly higher than that in those patients without typical lesion (P " 0 . 0 5) . Multiple polypoid neoplasm accounted for 77.8% (1 068/1 372) of endometrial polypoid lesion diagnosed by hysteroscopy, while the coincidence rate in those patients was 98,0% (1 047/1 068), Conclusions: The diagnostic coincidence rate of hysteroscopy and histopathology is high in those patients with typical endometrial neoplasm under hysteroscopy. The hysteroscopy combined with histopathology is the golden standard for the diagnosis of endometrial lesion. [ABSTRACT FROM AUTHOR]

Endometrial polyps is one of the most common gynecological diseases, which can induce menstrual period extended, postmenopausal bleeding, infertility and other clinical symptoms. After treatment, endometrial polyps also are easy to relapse, have certain malignant transformation rate, whose etiology and pathogenesis is not clear. In recent research, this disease is correlated with genetic factors, local imbalanced steroid hormone receptor, proliferation and apoptosis, chronic inflammatory stimulation, certain drugs and cell factor. Age, postmenopausal, anomalistic uterine bleeding, use of tamoxifen, obesity, hypertension, diabetes mellitus may involved in its progression. Through translational ultrasonography, sonohysterography, hysteroscopy, uterine iodine oil imaging play an important role in its treatment process. Now from the epidemiology, pathogenesis, clinical symptoms, diagnosis and treatment, recurrence, malignant related factors, prevention of endometrial polyps, we do a review, for we can more inclusively and more correctly promulgate the mechanism and characteristics of endometrial polyps, and then we can better guide further clinical research and therapy. [ABSTRACT FROM AUTHOR]

Endometriosis (EMs) is defined by the presence of visible endometrial implants outside the uterus, mostly occurred in the pelvic organs. The cyclical bleeding of ectopic endometrial lesions leads to serious pelvic pain and infertility of women. EMs is widely viewed as an estrogen-dependent disorder. Progesterone is the classic drug to antagonist estrogen. But in the clinical practice, the majority of the endometriosis patients show low reaction or non-reaction on progestin therapy. Attenuation of progesterone response at the level of the endometrium may be expected to have a deleterious impact on endometrial receptivity and fertility. These phenomena are called progesterone resistance of EMs. The progesterone resistance mechanism involves the defect of the progesterone receptor (PR), the change of progesterone receptor co-regulators and the genetic and environmental factors as well as ERα/ERβ. The aim of this review is to highlight recent findings regarding the progesterone resistance mechanisms and to provide theoretical basis for overcoming progesterone resistance. [ABSTRACT FROM AUTHOR]