CD24 promotes the proliferation and inhibits the apoptosis of cervical cancer cells in vitro

Zhang, Pei; Zhu, Guangchao; Huo, Xiao-Lei; Liao, Shan; He, Junyu; Long, Yuehua; Yi, Hong; Xiao, Songshu; Yi, Wei; Chen, Pan; Li, Xiaoling; Li, Guiyuan; Zhou, Yanhong

doi:10.3892/or.2015.4521

Cited by 21 publications

(14 citation statements)

References 32 publications

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“…CD24 is overexpressed in various human malignancies (cervical, gliomas, breast, pancreas, esophageal squamous cell carcinoma, gastric, bladder, and colorectal). In in-vivo and in-vitro cancer models, it was suggested that CD24 promotes colorectal, cervical, and breast cancer cell proliferation [4][5][6][7]. CD24 is also considered a marker for cancer [8] and thus was proposed as a diagnostic tool for cancer [9].…”

Section: Introductionmentioning

confidence: 99%

Behavioral Characterizing of CD24 Knockout Mouse—Cognitive and Emotional Alternations

Nitzan

Toledano

Shapira

et al. 2021

JPM

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CD24 is a small, glycophosphatidylinositol-anchored cell surface protein, mostly investigated with respect to cancer, inflammation, and autoimmune diseases. CD24 knockdown or inhibition has been used to test various biochemical mechanisms and neurological conditions; however, the association between CD24 and behavioral phenotypes has not yet been examined. This study aims to characterize cognitive and emotional functions of CD24 knockout mice (CD24−/−) compared with CD24 wild-type mice at three time-points: adolescence, young adulthood, and adulthood. Our results show that CD24−/− mice exhibited better cognitive performance and less anxiety-like behavior compared with WT mice, with no effect on depression-like behavior. This phenotype was constant from childhood (2 months old) to adulthood (6 months old). The results from our study suggest that CD24 may influence important behavioral aspects at the whole-organism level, which should be taken into consideration when using CD24 knockout models.

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Section: Introductionmentioning

confidence: 99%

Behavioral Characterizing of CD24 Knockout Mouse—Cognitive and Emotional Alternations

Nitzan

Toledano

Shapira

et al. 2021

JPM

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“…Numerous proteins, including cluster of differentiation (CD)44, CD24, CD38, Fos-related antigen-1, heat shock protein β-1 and transcription factor SOX-9, have been implicated in cervical cancer, and dysregulation of these proteins is closely associated with the occurrence and outcome of cervical cancer (34)(35)(36)(37)(38)(39). However, the etiology of cervical carcinoma remains elusive.…”

Section: Discussionmentioning

confidence: 99%

TNFAIP8 promotes cisplatin resistance in cervical carcinoma cells by inhibiting cellular apoptosis

Su-xia

et al. 2019

Oncol Lett

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Cervical cancer is the second most prevalent malignant tumor in women worldwide. Failure of successful treatment is most prevalent in patients with the metastatic disease and the chemotherapy refractory disease. Tumor necrosis factor α-induced protein 8 (TNFAIP8) serves as an anti-apoptotic and pro-oncogenic protein, and is associated with cancer progression and poor prognosis in a number of different cancer types. However, the physiological and pathophysiological roles of TNFAIP8 in cervical carcinogenesis and development remain poorly understood. In the present study, it was demonstrated that TNFAIP8 protein expression levels were significantly increased in cervical cancer tissues compared with the non-tumor adjacent tissues using immunohistochemistry. Additionally, it was demonstrated that TNFAIP8 overexpression is associated with cisplatin resistance. Furthermore, depletion of TNFAIP8 impaired HeLa cell proliferation and viability in vitro, improved cisplatin sensitivity, and promoted cisplatin-induced cellular apoptosis and death. Subsequent mechanistic analysis demonstrated that TNFAIP8 silencing promoted caspase-8/-3 activation and p38 phosphorylation in HeLa cells treated with cisplatin, whereas apoptosis regulator B-cell lymphoma-2 expression was inhibited with TNFAIP8-silenced HeLa cells following treatment with cisplatin. These data suggested that TNFAIP8 serves as an anti-apoptotic protein against cisplatin-induced cell death, which eventually leads to chemotherapeutic drug-treatment failure. Therefore, the present data suggested that TNFAIP8 may be a promising therapeutic target for the treatment of cervical cancer.Abbreviations: TNFAIP8, tumor necrosis factor α-induced protein 8; MAPK, mitogen-activated protein kinase; CDDP, Cis-diamminedichloroplatinum

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“…CD24, an adhesive molecule and one of molecular biomarkers of cancer stem cells, is associated with cancer cell proliferation and migration [ 34 , 35 ], and cells with CD24 expression may be the cancer-initiating cells that promote tumor migration and metastasis [ 36 – 38 ]. Wang and his colleagues reported that CD24 expression increased gradually in samples of normal gastric mucosa, non-atrophic chronic gastritis, chronic atrophic gastritis (CAG), CAG with intestinal metaplasia, dysplasia and GC [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of AQP3 and CD24 as biomarkers for carcinogenesis of gastric intestinal metaplasia

et al. 2017

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Gastric intestinal metaplasia (GIM) is a precancerous gastric carcinoma (GC) lesion with pivotal roles in carcinogenesis. CD24, LGR5 and Ki67 are expressed in GIM; we previously demonstrated that aquaporin 3 (AQP3) is expressed in goblet cells and is positively correlated with GIM severity. However, the relationships of AQP3 with GIM classification and with other proteins, and their roles in the transition from GIM to gastric carcinoma (GC) remain unknown. Sixteen patients with intestinal-type GC were enrolled in this study. GIM was determined according to the updated Sydney system; GIM classification was determined via HID-AB staining, and AQP3, CD24, LGR5 and Ki67 expression were determined by immunohistochemistry. Type III GIM was more prevalent around the GC and displayed a positive association with GIM severity. CD24 was found in GIM, but LGR5 and Ki67 were found in tissues regardless of GIM. AQP3 expression showed significant correlation to type III GIM. CD24 expression was correlated with the marked GIM and incomplete GIM, while LGR5 expression decreased with GIM aggravation and did not have relationship with classification of GIM. However, Ki67 presented no association with GIM grade or classification. These observations identify AQP3 and CD24 as biomarkers for carcinogenesis of GIM, and may provide a precise strategy for screening at-risk candidates with GIM.

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CD24 promotes the proliferation and inhibits the apoptosis of cervical cancer cells in vitro

Cited by 21 publications

References 32 publications

Behavioral Characterizing of CD24 Knockout Mouse—Cognitive and Emotional Alternations

Behavioral Characterizing of CD24 Knockout Mouse—Cognitive and Emotional Alternations

TNFAIP8 promotes cisplatin resistance in cervical carcinoma cells by inhibiting cellular apoptosis

Identification of AQP3 and CD24 as biomarkers for carcinogenesis of gastric intestinal metaplasia

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