Correlation of CD24 expression with histological grading and TNM staging of retinoblastoma

Ishaq, Syed Muhammad; Kehar, Shahnaz Imdad; Zafar, Shahid; Hasan, Syed Furqan

doi:10.12669/pjms.321.8828

Cited by 4 publications

(4 citation statements)

References 11 publications

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“…Among the patients, 36 had RB in one eye and 20 had RB in both eyes. According to the degrees of optic nerve invasion, the patients were divided into four groups according to tumor necrosis metastasis staging system: N0, RB did not invade optic nerves (n=9); N1, RB invaded optic papilla, but did not exceed sieve plate (n=6); N2, RB passed through sieve plate, but did not invade the end of optic nerves (n=25); and N3, RB cells were identified at the end of optic nerves (n=16) ( 21 ). Depending on whether RB cells were arranged into a Flexner-Winterstein rose ring, RB tissues were stratified into a high-differentiation group (n=39 cases) and a poor-differentiation group (n=17).…”

Section: Methodsmentioning

confidence: 99%

MicroRNA‑106b promotes the proliferation, migration and invasion of retinoblastoma cells by inhibiting the expression of ZBTB4 protein

Wang

Xiangrong

2018

Exp Ther Med

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The present study investigated the function of microRNA (miR)-106b in the proliferation, migration and invasion of retinoblastoma (RB) cells, and aimed to elucidate the underlying mechanism. A total of 56 patients with RB were enrolled in the present study. The expression of miR-106b in RB tissues was measured by reverse transcription quantitative polymerase chain reaction. After transfection with miR-106b mimics or miR-106b inhibitor, a Cell-Counting kit-8 assay was used to determine the proliferation of WERI-Rb-1 cells and a Transwell assay was employed to measure the migration and invasion of the cells. Western blot analysis was performed to determine the expression of zinc finger and BTB domain containing 4 (ZBTB4) protein. By silencing or overexpression of ZBTB4 protein, the biological functions of ZBTB4 in WERI-Rb-1 cells were studied. A dual luciferase reporter assay was performed to test whether ZBTB4 was a target gene of miR-106b. The expression of miR-106b in RB tissues was elevated and closely associated with the severity of the disease. Overexpression of miR-106b increased but inhibition of miR-106b expression decreased the proliferation, migration and invasion abilities of WERI-Rb-1 cells. In addition, overexpression of miR-106b decreased but inhibition of miR-106b expression increased ZBTB4 protein expression in WERI-Rb-1 cells. Similarly, overexpression of ZBTB4 reduced but inhibition of ZBTB4 expression promoted the proliferation, migration and invasion of WERI-Rb-1 cells. Finally, miR-106b regulated the expression of ZBTB4 by binding to the 3′-untranslated region of the ZBTB4 gene. The present study demonstrated that increased expression of miR-106b in RB tissues is positively associated with the metastasis and differentiation of RB cells. As an oncogene, miR-106b promotes the proliferation, migration and invasion of WERI-Rb-1 cells by inhibiting the expression of ZBTB4 protein.

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Section: Methodsmentioning

confidence: 99%

MicroRNA‑106b promotes the proliferation, migration and invasion of retinoblastoma cells by inhibiting the expression of ZBTB4 protein

Wang

Xiangrong

2018

Exp Ther Med

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“…Negative controls were prepared by omitting the primary antibody. Spleen tissues were used as positive controls for both antibodies (23) .…”

Section: Measurement Of the Depth Of Invasion (Doi)mentioning

confidence: 99%

Therapeutic potential of epigallocatechin-3-gallate on cancer stem cells of DMBA induced hamster buccal pouch carcinoma

Al-Dosoki elagouz,

M.Zahran,

Zouair

et al. 2023

Al-Azhar Journal of Dental Science

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Objective:The aim of the present study was directed to investigate the therapeutic potential of epigallocatechin-3gallate (EGCG) on cancer stem cell(s) (CSC(s)) of DMBA induced hamster buccal pouch (HBP) carcinoma. Subjects and methods: thirty Syrian male hamsters were divided into three group(s) (G(s)),10 each. GI: negative control, left untreated. The right pouches of those in GII and GII were painted with DMBA (3times /a week/ 14 weeks). GII: positive control, not received other treatment. GIII was injected with intraperitoneally with EGCG. After termination of the experiment, gross observations were recorded, then, the animals were euthanized, all pouches were surgically excised and bisected. The first piece was prepared, fixed and processed for hematoxylin and eosin (H&E) stain examination and immunohistochemical (IHC) staining utilizing CD44 and CD24. The other piece of the fresh tissue was used for flow cytometric (FCM) assessment for identification of CSCs using CD44&CD24 fluorophore-antibodies, then, apoptosis assay of the identified CD44+CD24-CSCs was employed. Results: the results of GIII revealed some variability compared to those observed in GII in gross observations as well as when utilizing H&E stain, CD44 & CD24 IHC and FCM assessment of CSCs. CD44 &CD24 IHC revealed highly significant difference between GII and GIII, (p value > 0.001). CSCs identification, CD44+CD24-& CD44+CD24+revealed highly significant difference between GII and GIII, (p value > 0.05)}. The CD44+CD24-CSCs apoptosis recorded highly significant difference between GII and GIII (p value < 0.001). Conclusion: EGCG significantly inhibits tumor progression and induces apoptosis in CSC of HBP carcinoma.

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“…Similarly, lncRNA XIST promotes autophagy in RB tumour cells. XIST silencing suppresses autophagy, tumour proliferation, and enhances apoptosis, additionally sensitizing RB cells to vincristine [ 138 ], the efficacy of which is often limited because of chemoresistance. In this respect, it has recently been discovered that CD24, a plasma membrane GPI-anchored protein being overexpressed in RB and representing a poor prognostic factor in several tumours including RB [ 139 ], impairs RB sensitivity to vincristine by means of promoting autophagy activation [ 140 ].…”

Section: Autophagy In Childhood Brain Tumoursmentioning

confidence: 99%

Recent Advances in Understanding the Role of Autophagy in Paediatric Brain Tumours

et al. 2021

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Autophagy is a degradative process occurring in eukaryotic cells to maintain homeostasis and cell survival. After stressful conditions including nutrient deprivation, hypoxia or drugs administration, autophagy is induced to counteract pathways that could lead to cell death. In cancer, autophagy plays a paradoxical role, acting both as tumour suppressor—by cleaning cells from damaged organelles and inhibiting inflammation or, alternatively, by promoting genomic stability and tumour adaptive response—or as a pro-survival mechanism to protect cells from stresses such as chemotherapy. Neural-derived paediatric solid tumours represent a variety of childhood cancers with unique anatomical location, cellular origins, and clinical presentation. These tumours are a leading cause of morbidity and mortality among children and new molecular diagnostics and therapies are necessary for longer survival and reduced morbidity. Here, we review advances in our understanding of how autophagy modulation exhibits antitumor properties in experimental models of paediatric brain tumours, i.e., medulloblastoma (MB), ependymoma (EPN), paediatric low-grade and high-grade gliomas (LGGs, HGGs), atypical teratoid/rhabdoid tumours (ATRTs), and retinoblastoma (RB). We also discuss clinical perspectives to consider how targeting autophagy may be relevant in these specific paediatric tumours.

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Correlation of CD24 expression with histological grading and TNM staging of retinoblastoma

Cited by 4 publications

References 11 publications

MicroRNA‑106b promotes the proliferation, migration and invasion of retinoblastoma cells by inhibiting the expression of ZBTB4 protein

MicroRNA‑106b promotes the proliferation, migration and invasion of retinoblastoma cells by inhibiting the expression of ZBTB4 protein

Therapeutic potential of epigallocatechin-3-gallate on cancer stem cells of DMBA induced hamster buccal pouch carcinoma

Recent Advances in Understanding the Role of Autophagy in Paediatric Brain Tumours

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