Increased expression of ZNF 703 in breast cancer tissue: An opportunity for RNAi–NSAID combinatorial therapy

Marzbany, Marzieh; Bishayee, Anupam; Rasekhian, Mahsa

doi:10.1002/bab.1790

Cited by 10 publications

(10 citation statements)

References 42 publications

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“…Recently, Mishra et al revealed that methylation of ZNF genes could serve as a molecular clustering basis for pancreatic cancer ( Mishra and Guda, 2017 ). A few analyses have focused on the clinical significance of ZNF genes’ expression on drug resistance ( Lee et al, 2013 ; Marzbany et al, 2019 ). Several functional studies on the role of mediating chemoresistance point out that ZNF genes may induce chemoresistance via DNA repair and activation of resistance genes’ transcription ( Rink et al, 2013 ; Chen et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Systematic Investigation of DNA Methylation Associated With Platinum Chemotherapy Resistance Across 13 Cancer Types

Sun

et al. 2021

Front. Pharmacol.

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Background: Platinum resistance poses a significant problem for oncology clinicians. As a result, the role of epigenetics and DNA methylation in platinum-based chemoresistance has gained increasing attention from researchers in recent years. A systematic investigation of aberrant methylation patterns related to platinum resistance across various cancer types is urgently needed.Methods: We analyzed the platinum chemotherapy response-related methylation patterns from different perspectives of 618 patients across 13 cancer types and integrated transcriptional and clinical data. Spearman’s test was used to evaluate the correlation between methylation and gene expression. Cox analysis, the Kaplan-Meier method, and log-rank tests were performed to identify potential risk biomarkers based on differentially methylated positions (DMPs) and compare survival based on DMP values. Support vector machines and receiver operating characteristic curves were used to identify the platinum-response predictive DMPs.Results: A total of 3,703 DMPs (p value < 0.001 and absolute delta beta >0.10) were identified, and the DMP numbers of each cancer type varied. A total of 39.83% of DMPs were hypermethylated and 60.17% were hypomethylated in platinum-resistant patients. Among them, 405 DMPs (Benjamini and Hochberg adjusted p value < 0.05) were found to be associated with prognosis in tumor patients treated with platinum-based regimens, and 664 DMPs displayed the potential to predict platinum chemotherapy response. In addition, we defined six DNA DMPs consisting of four gene members (mesothelin, protein kinase cAMP-dependent type II regulatory subunit beta, msh homeobox 1, and par-6 family cell polarity regulator alpha) that may have favorable prognostic and predictive values for platinum chemotherapy.Conclusion: The methylation-transcription axis exists and participates in the complex biological mechanism of platinum resistance in various cancers. Six DMPs and four associated genes may have the potential to serve as promising epigenetic biomarkers for platinum-based chemotherapy and guide clinical selection of optimal treatment.

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Section: Discussionmentioning

confidence: 99%

Systematic Investigation of DNA Methylation Associated With Platinum Chemotherapy Resistance Across 13 Cancer Types

Sun

et al. 2021

Front. Pharmacol.

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“…Interestingly, Marzbany et al disclosed that there was an increased expression of ZNF703 in breast cancer tissues and cells. 26 Then, we conducted dual luciferase reporter assay to prove the prediction, and Western blot assay implicated that the level of ZNF703 was negatively regulated by miR-491-5p. Furthermore, ZNF703 rescued the activities of miR-491-5p overexpression on proliferation, apoptosis, migration and invasion.…”

Section: Discussionmentioning

confidence: 99%

“…25 Besides, Marzbany et al revealed that the silencing of ZNF703 obviously induced apoptosis of breast cancer cells combined with ibuprofen, which provided a combinatorial therapy for breast cancer. 26 Despite so many researches of ZNF703 in breast cancer, the interaction among H19, miR-491-5p and ZNF703 has not been illuminated.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Non-Coding RNA H19 Promotes Proliferation, Migration and Invasion and Inhibits Apoptosis of Breast Cancer Cells by Targeting miR-491-5p/ZNF703 Axis</p>

Wang

et al. 2020

CMAR

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Background: Breast cancer is one of the most common cancers worldwide. Long noncoding RNAs and microRNAs act as important regulators in human cancers. This study aims to explore the molecular mechanism among H19, miR-491-5p and zinc finger 703 (ZNF703) in breast cancer. Materials and Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to detect the expression of H19, miR-491-5p and ZNF703. Cell Counting Kit 8 (CCK-8) assay was performed to evaluate cell proliferation. Cell apoptosis was assessed by flow cytometry assay. The number of migrated and invaded cells was counted by transwell assay. Dual luciferase reporter assay was carried out to test luciferase activity. Protein level of ZNF703 was measured by Western blot assay. Results: H19 was highly expressed in breast tissues and cells. H19 knockdown inhibited proliferation, induced apoptosis and blocked migration and invasion. Moreover, H19 bound to miR-491-5p and negatively regulated miR-491-5p expression. MiR-491-5p inhibition abrogated the activities of proliferation, apoptosis, migration and invasion affected by H19 knockdown. Furthermore, miR-491-5p directly targeted ZNF703 and inversely modulated ZNF703 expression. ZNF703 up-regulation rescued the effects of miR-491-5p overexpression on proliferation, apoptosis, migration and invasion. In addition, H19 knockdown reduced ZNF703 expression by targeting miR-491-5p/ZNF703 axis. Conclusion: H19 promoted proliferation, migration and invasion and retarded apoptosis of breast cancer cells via sponging miR-491-5p to down-regulate ZNF703 expression.

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“…This may be attributed to the difference between these cell lines in their mechanism of anticancer resistance. Some cancer origins induce significant activation of inflammatory signals such as NFkB pathway and others have high expression of antiapoptotic proteins that may require other strategies for combination therapies to enhance cancer cell sensitivity [41‐44].…”

Section: Discussionmentioning

confidence: 99%

Repurposing of quinoline alkaloids identifies their ability to enhance doxorubicin‐induced sub‐G0/G1 phase cell cycle arrest and apoptosis in cervical and hepatocellular carcinoma cells

El-Mesery

Seher

El-Shafey

et al. 2020

Biotech and App Biochem

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The ability of quinoline alkaloids (cinchonine, cinchonidine, quinine, and quinidine) to sensitize different human cancer cell lines to doxorubicin (DOX)‐induced cell death was evaluated. Cell viability was analyzed using 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay and the alkaloids ability to enhance DOX‐induced apoptosis was explored using Western blotting analysis. Also, flow cytometry was applied to analyze cell fractions in the different cell cycle phases. All alkaloids showed a significant enhancement of DOX‐induced cell death in HeLa and HepG2 cell lines. The chemosensitizing activity of the quinoline alkaloids was attributed to the induction of apoptosis as indicated by splitting of caspase‐3 and its substrate poly (ADP‐ribose) polymerase (PARP). In addition, there was an increase in the cell fractions in sub‐G0/G1 phase in case of DOX combination with the alkaloids. This study proves the ability of the quinoline alkaloids to enhance DOX‐induced apoptotic cell death in human cervical and hepatocellular carcinoma cells.

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Increased expression of ZNF 703 in breast cancer tissue: An opportunity for RNAi–NSAID combinatorial therapy

Cited by 10 publications

References 42 publications

Systematic Investigation of DNA Methylation Associated With Platinum Chemotherapy Resistance Across 13 Cancer Types

Systematic Investigation of DNA Methylation Associated With Platinum Chemotherapy Resistance Across 13 Cancer Types

<p>Long Non-Coding RNA H19 Promotes Proliferation, Migration and Invasion and Inhibits Apoptosis of Breast Cancer Cells by Targeting miR-491-5p/ZNF703 Axis</p>

Repurposing of quinoline alkaloids identifies their ability to enhance doxorubicin‐induced sub‐G0/G1 phase cell cycle arrest and apoptosis in cervical and hepatocellular carcinoma cells

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