Cell cycle‐dependent regulation of cytoglobin by Skp2

John, Rince; Atri, Yama; Chand, Vaibhav; Jaiswal, Neha; Raj, Kritika; Nag, Alo

doi:10.1002/1873-3468.12864

Cited by 10 publications

(6 citation statements)

References 52 publications

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“…For example, the downstream mechanism of SKP2 in RB cell growth has not been annotated. Some reports demonstrating mechanisms of SKP2 in regulating cell growth attracted our great interest, [30][31][32][33] and we projected to run mechanical assays to probe the downstream events of SKP2 in promoting RB cell growth.…”

Section: Discussionmentioning

confidence: 99%

SKP2, positively regulated by circ_ODC1/miR‐422a axis, promotes the proliferation of retinoblastoma

Wang

Zhang

et al. 2019

J of Cellular Biochemistry

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Retinoblastoma (RB) is the most common intraocular malignancy in infants and children. S‐phase kinase‐associated protein 2 (SKP2) has been unmasked as an oncogene in a great many of carcinomas. The biologic function and the detailed molecular mechanism of SKP2 in RB need to be better understood. In this study, real‐time quantitative polymerase chain reaction and Western blot showed the ectopic expression of SKP2 in RB tissues and cell lines. Loss of function assays showed the attenuated cell proliferation in RB as a result of SKP2 knockdown. In addition, bioinformatics analysis predicted the interaction between SKP2 and miR‐422a. Luciferase reporter assay and Pearson's correlation analysis validated the negative correlation between miR‐422a and SKP2. MiR‐422a overexpression led to a decline of SKP2 expression and cell growth in RB. The binding capacity between miR‐422a and circ_ODC1 was also predicted by bioinformatics analysis. Pearson's correlation analysis and luciferase reporter assay confirmed that circ_ODC1 is negatively correlated with miR‐422a. Silencing circ_ODC1 resulted in a rise in miR‐422a expression and RB cell growth. Moreover, reduced cell growth was restored by SKP2 overexpression. In a word, SKP2, induced by circ_ODC1 and miR‐422a, promotes RB proliferation. Our new findings in this research might expedite the discovery of novel prognostic markers and therapeutic targets of RB.

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Section: Discussionmentioning

confidence: 99%

SKP2, positively regulated by circ_ODC1/miR‐422a axis, promotes the proliferation of retinoblastoma

Wang

Zhang

et al. 2019

J of Cellular Biochemistry

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“…Protein degradation assay was performed as described previously (80). In brief, cells were transfected with the desired expression vectors and 16 h post transfection, they were (which was not certified by peer review) is the author/funder.…”

Section: Cycloheximide Chase Assaymentioning

confidence: 99%

“…HEK293T cells were transfected with vectors expressing Flag-Cdh1, HA-Ub and Myc-E7 or other constructs as indicated in the figures, using calcium phosphate method. As discussed in our earlier publication (80), after 36 h of transfection, cells were treated with 20 µM MG132 (Sigma, St. Louis, MO) for 5 h. MG132 (Z-Leu-Leu-Leu-al) is a peptide aldehyde, which effectively blocks the proteolytic activity of the 26S proteasome complex (81). It is a specific, potent, reversible, and cell-permeable proteasome inhibitor.…”

Section: In Vivo Ubiquitination Assaymentioning

confidence: 99%

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The anaphase-promoting complex/cyclosome co-activator, Cdh1, is a novel target of human papillomavirus 16 E7 oncoprotein in cervical oncogenesis

et al. 2022

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The transforming properties of the high risk human papillomavirus (HPV) E7 oncoprotein are indispensable for driving the virus life cycle and pathogenesis. Besides inactivation of the retinoblastoma family of tumor suppressors as part of its oncogenic endeavors, E7-mediated perturbations of eminent cell cycle regulators, checkpoint proteins and proto-oncogenes are considered to be the tricks of its transformative traits. However, many such critical interactions are still unknown. In the present study, we have identified the anaphase promoting complex/cyclosome (APC) co-activator, Cdh1, as a novel interacting partner and a degradation target of E7. We found that HPV16 E7-induced inactivation of Cdh1 promoted abnormal accumulation of multiple Cdh1 substrates. Such a mode of deregulation possibly contributes to HPV-mediated cervical oncogenesis. Our mapping studies recognized the carboxyl-terminal zinc finger motif of E7 to associate with Cdh1 and interfere with the timely degradation of FoxM1, a bona fide Cdh1 substrate and a potent oncogene. Importantly, the E7 mutant with impaired interaction with Cdh1 exhibited defects in its ability for overriding typical cell cycle transition and oncogenic transformation, thereby validating the functional and pathological significance of the E7-Cdh1 axis during cervical carcinoma progression. Altogether, the findings from our study discover a unique nexus between E7 and APC/C-Cdh1, thereby adding to our understanding of the mechanism of E7-induced carcinogenesis and provide a promising target for the management of cervical carcinoma.

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“…BrdU assay was carried out using the protocol published earlier (80). Briefly, cells were seeded with coverslips in a 12-well plate so that cells attain around 80% confluency the following day and allowed to grow in a 37ºC humidified CO 2 incubator overnight.…”

Section: Brdu Immunofluorescencementioning

confidence: 99%

The Anaphase Promoting Complex/ cyclosome co-activator, Cdh1, is a novel target of human Papillomavirus 16 E7 oncoprotein in cervical oncogenesis

Jaiswal

Nandi

Cheema

et al. 2021

Preprint

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The transforming properties of the high risk human papillomavirus E7 oncoprotein are indispensable for driving the virus life cycle and pathogenesis. Besides inactivation of retinoblastoma (Rb) family of tumor suppressors as part of its oncogenic endeavors, E7-mediated perturbations of eminent cell cycle regulators, checkpoint proteins and proto-oncogenes are considered to be the tricks of its transformative traits. However, many such critical interactions are still unknown. In the present study, we have identified the anaphase promoting complex/ cyclosome (APC/C) co-activator, Cdh1, as a novel interacting partner and a degradation target of E7. We found that HPV16 E7-induced inactivation of Cdh1 promoted abnormal accumulation of multiple Cdh1 substrates. Such a mode of deregulation possibly contributes to HPV-mediated cervical oncogenesis. Our mapping studies recognized the carboxyl-terminal zinc finger motif of E7 to associate with Cdh1 and interfere with the timely degradation of FoxM1, a bona fide Cdh1 substrate and a potent oncogene. Importantly, the E7 mutant with impaired interaction with Cdh1 exhibited defects in its ability for overriding typical cell cycle transition and oncogenic transformation, thereby validating the functional and pathological significance of the E7-Cdh1 axis during cervical carcinoma progression. Altogether, the findings from our study discover a unique nexus between E7 and APC/C-Cdh1, thereby adding to our understanding of the mechanism of E7-induced carcinogenesis and provide a promising target for the management of cervical carcinoma.

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Cell cycle‐dependent regulation of cytoglobin by Skp2

Cited by 10 publications

References 52 publications

SKP2, positively regulated by circ_ODC1/miR‐422a axis, promotes the proliferation of retinoblastoma

SKP2, positively regulated by circ_ODC1/miR‐422a axis, promotes the proliferation of retinoblastoma

The anaphase-promoting complex/cyclosome co-activator, Cdh1, is a novel target of human papillomavirus 16 E7 oncoprotein in cervical oncogenesis

The Anaphase Promoting Complex/ cyclosome co-activator, Cdh1, is a novel target of human Papillomavirus 16 E7 oncoprotein in cervical oncogenesis

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