rs6426881 in the 3'-UTR of PBX1 is involved in breast and gastric cancers via altering the binding potential of miR-522-3p

Mohammadi, Maryam; Salehzadeh, Ali; Sasani, Soheila Talesh; Tarang, Alireza

doi:10.1007/s11033-021-06756-5

Cited by 5 publications

(5 citation statements)

References 44 publications

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“…Previous research has showed that pre-B cell leukemia homeobox-1 (PBX1) was involved in many important developmental programs, and its dysregulation associated with multifactorial disorders (Veiga et al 2021 ). Though changing the regulatory miR-522-3p affinity to PBX1 3'-UTR, the rs6426881 T allele at PBX1 3′-UT is prominently correlated with breast carcinoma and gastric carcinoma (Mohammadi et al 2021 ). Through targeting PBX1, microRNA-181 regulates posterior longitudinal ligament ossification (Liu et al 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Small nucleolar RNA Snora73 promotes psoriasis progression by sponging miR-3074-5p and regulating PBX1 expression

Zhang,

Guo,

Zhang

et al. 2024

Funct Integr Genomics

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Chronic psoriasis is a kind of immune-mediated skin illness and the underlying molecular mechanisms of pathogenesis remain incompletely understood. Here, we used small RNA microarray assays to scan the differential expressed RNAs in psoriasis patient samples. The downstream miRNAs and its targets were predicted using bioinformatics analysis from online bases and confirmed using fluorescence in situ hybridization and dual‑luciferase report gene assay. Cell ability of proliferation and migration were detected using CCK-8 and transwell assays. The results showed that a new snoRNA Snora73 was upregulated in psoriasis patient samples. Overexpression of Snora73 significantly increased psoriasis cells viability and migration, while knockdown of Snora73 got the opposite results. Mechanistically, our results showed that Snora73 acted as a sponge for miR-3074-5p and PBX1 is a direct target of miR-3074-5p in psoriasis cells. Furthermore, miR-3074-5p suppressed psoriasis cell proliferation and migration, while PBX1 promoted cell proliferation and migration in psoriasis. Collectively, these findings reveal a crucial role of Snora73 in progression of psoriasis through miR-3074-5p/PBX1 signaling pathway and suggest a potential therapeutic strategy.

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Section: Discussionmentioning

confidence: 99%

Small nucleolar RNA Snora73 promotes psoriasis progression by sponging miR-3074-5p and regulating PBX1 expression

Zhang,

Guo,

Zhang

et al. 2024

Funct Integr Genomics

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“…Previously, miR-522-3p showed aberrant expression in GC cells [ 25 ]. Nevertheless, its biological role in GC cells remains elusive.…”

Section: Resultsmentioning

confidence: 99%

“…miR-216b suppresses GC proliferation and migration through modulating PARK7 [ 24 ]. Previously, microarrays revealed that miR-522-3p was presented as a differential expression in GC [ 25 ]. Cancer-associated fibroblasts secrete miR-522, which represses ferroptosis and facilitates chemoresistance in GC cells [ 26 ].…”

Section: Introductionmentioning

confidence: 99%

MiR-522-3p Targets Transcription Factor 4 to Overcome Cisplatin Resistance of Gastric Cells

Guo¹,

Xue²,

Ni³

et al. 2022

Journal of Oncology

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Gastric cancer (GC) is a malignancy originating from gastric epithelial tissue. Chemoresistance to cisplatin (DDP) often leads to chemotherapy failure in GC. Previously, miR-522 was found to be associated with chemoresistance in GC cells. Thus, we attempted to clarify miR-522-3p’s role underlying chemoresistance of GC cells. RT-qPCR measured the miR-522-3p levels in untreated and DDP-treated AGS cells. RT-qPCR and Western blotting detected transcription factor 4 (TCF4) mRNA and protein levels in GC cells. AGS and AGS/DDP cell proliferation were detected by the colony formation assay. Flow cytometry analysis detected AGS and AGS/DDP cell apoptosis. Bioinformatics and dual luciferase reporter assays predicted and verified the relationship between miR-522-3p and TCF4. Rescue experiments further clarified the regulatory patterns of miR-522-3p/TGF4 in GC cells. miR-522-3p presented a downregulation in GC cells and was positively affected by DDP. TCF4 presented elevation in GC cells and was negatively affected by DDP. Mechanistically, miR-522-3p targeted TCF4 to suppress TCF4 gene expression. miR-522-3p overexpression suppressed GC cell proliferation and resistance to DDP and GC cell apoptosis was facilitated. TCF4 overexpression facilitated GC cell proliferation and resistance to DDP while repressing GC cell apoptosis. TCF4 elevation rescued changes in GC cell proliferation, apoptosis, and chemoresistance due to miR-522-3p overexpression. To sum up, miR-522-3p suppresses GC cell malignancy and resistance to DDP via targeting TCF4. Our research may provide a new biomarker for GC diagnosis and a novel direction for GC chemotherapy.

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“…Micro‐ARNs (miRNA) are also of importance in regulating mRNA levels: 3′UTR variations affecting miRNA binding sites are implicated in human diseases such as Tourette's syndrome (review by Kawahara [2014]). Very recently, an SNP in the 3′UTR sequence of PBX1 was linked to poor prognosis in breast and gastric cancers, by alteration of the regulatory affinity of miR‐522‐3p (Mohammadi et al, 2021). Thus, the occurrence of aberrant miRNA binding sites in PBX1 could also play a role in the milder phenotypes caused by missense variants.…”

Section: Genotype‐phenotype Variations In Pbx1‐mutated Patientsmentioning

confidence: 99%

The TALE never ends: A comprehensive overview of the role of PBX1, a TALE transcription factor, in human developmental defects

et al. 2022

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PBX1 is a highly conserved atypical homeodomain transcription factor (TF) belonging to the TALE (three amino acid loop extension) family. Dimerized with other TALE proteins, it can interact with numerous partners and reach dozens of regulating sequences, suggesting its role as a pioneer factor. PBX1 is expressed throughout the embryonic stages (as early as the blastula stage) in vertebrates. In human, PBX1 germline variations are linked to syndromic renal anomalies (CAKUTHED). In this review, we summarized available data on PBX1 functions, PBX1‐deficient animal models, and PBX1 germline variations in humans. Two types of genetic alterations were identified in PBX1 gene. PBX1 missense variations generate a severe phenotype including lung hypoplasia, cardiac malformations, and sexual development defects (DSDs). Conversely, truncating variants generate milder phenotypes (mainly cryptorchidism and deafness). We suggest that defects in PBX1 interactions with various partners, including proteins from the HOX (HOXA7, HOXA10, etc.), WNT (WNT9B, WNT3), and Polycomb (BMI1, EED) families are responsible for abnormal proliferation and differentiation of the embryonic mesenchyme. These alterations could explain most of the defects observed in humans. However, some phenotype variability (especially DSDs) remains poorly understood. Further studies are needed to explore the TALE family in greater depth.

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rs6426881 in the 3'-UTR of PBX1 is involved in breast and gastric cancers via altering the binding potential of miR-522-3p

Cited by 5 publications

References 44 publications

Small nucleolar RNA Snora73 promotes psoriasis progression by sponging miR-3074-5p and regulating PBX1 expression

Small nucleolar RNA Snora73 promotes psoriasis progression by sponging miR-3074-5p and regulating PBX1 expression

MiR-522-3p Targets Transcription Factor 4 to Overcome Cisplatin Resistance of Gastric Cells

The TALE never ends: A comprehensive overview of the role of PBX1, a TALE transcription factor, in human developmental defects

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