Hybrid-polymerase chain reaction to identify novel target genes of miR-134 in paclitaxel resistant human ovarian carcinoma cells

Shuang, Ting; Wang, Min; Chang, Shuang

doi:10.3892/ol.2015.3137

Cited by 9 publications

(7 citation statements)

References 35 publications

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“…Prior to this study, C16ORF72 / TAPR1 was identified as a hit in human genome‐wide CRISPR‐Cas9 chemogenetic screens for sensitizers to ATR kinase inhibition or hydroxyurea (Hustedt et al., 2019; Benslimane et al., 2020). C16ORF72 / TAPR1 is also a target of miR‐134, a microRNA associated with tumorigenesis and chemo‐resistance (Shuang et al., 2015), and is associated with rare de novo CNVs in autism spectrum disorder (ASD) and schizophrenia (Levinson et al., 2011; Sanders et al., 2011). In our study, TAPR1 was identified as an interactor with HUWE1, and C16ORF72/TAPR1 also interacts with HUWE1 in previous high‐throughput mass spectrometry surveys (Hein et al., 2015; Thompson et al., 2014).…”

Section: Discussionmentioning

confidence: 99%

A novel p53 regulator, C16ORF72/TAPR1, buffers against telomerase inhibition

et al. 2021

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Telomere erosion in cells with insufficient levels of the telomerase reverse transcriptase (TERT), contributes to age‐associated tissue dysfunction and senescence, and p53 plays a crucial role in this response. We undertook a genome‐wide CRISPR screen to identify gene deletions that sensitized p53‐positive human cells to telomerase inhibition. We uncovered a previously unannotated gene, C16ORF72, which we term Telomere Attrition and p53 Response 1 (TAPR1), that exhibited a synthetic‐sick relationship with TERT loss. A subsequent genome‐wide CRISPR screen in TAPR1‐disrupted cells reciprocally identified TERT as a sensitizing gene deletion. Cells lacking TAPR1 or TERT possessed elevated p53 levels and transcriptional signatures consistent with p53 upregulation. The elevated p53 response in TERT‐ or TAPR1‐deficient cells was exacerbated by treatment with the MDM2 inhibitor and p53 stabilizer nutlin‐3a and coincided with a further reduction in cell fitness. Importantly, the sensitivity to treatment with nutlin‐3a in TERT‐ or TAPR1‐deficient cells was rescued by loss of p53. These data suggest that TAPR1 buffers against the deleterious consequences of telomere erosion or DNA damage by constraining p53. These findings identify C16ORF72/TAPR1 as new regulator at the nexus of telomere integrity and p53 regulation.

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Section: Discussionmentioning

confidence: 99%

A novel p53 regulator, C16ORF72/TAPR1, buffers against telomerase inhibition

et al. 2021

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“…explored the associations between miR-134 and SKOV3-TR30 cells, consistently discovering miR-134 expression was lower in drug-resistant ovarian cancer cells compared with no resistance. They also found eight potential target genes including VIM, a direct target, of miR-134 through PCR assay 100 . Regretfully, the underlying power of miR-134 in drug-resistant ovarian cancer has not been confirmed yet.…”

Section: Main Textmentioning

confidence: 99%

miR-134: A Human Cancer Suppressor?

Pan

Zhang

Sun

et al. 2017

Molecular Therapy - Nucleic Acids

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MicroRNAs (miRNAs) are small noncoding RNAs approximately 20–25 nt in length, which play crucial roles through directly binding to corresponding 3′ UTR of targeted mRNAs. It has been reported that miRNAs are involved in numerous of diseases, including cancers. Recently, miR-134 has been identified to dysregulate in handles of human cancers, such as lung cancer, glioma, breast cancer, colorectal cancer, and so on. Increasing evidence indicates that miR-134 is essential for human carcinoma and participates in tumor cell proliferation, apoptosis, invasion and metastasis, drug resistance, as well as cancer diagnosis, treatment, and prognosis. Nevertheless, its roles in human cancer are still ambiguous, and its mechanisms are sophisticated as well, referring to a variety of targets and signal pathways, such as STAT5B, KRAS, MAPK/ERK signal pathway, Notch pathway, etc. Herein, we review the crucial roles of miR-134 in scores of human cancers via analyzing latest investigations, which might provide evidence for cancer diagnose, treatment, prognosis, or further investigations.

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“…PRPF6 activates AR/AR-Vs to promote the progression of hepatocellular cancer and prostate cancer [22,23]. Our preliminary research found that PRPF6 may be a target gene of miR-134 mediating the regulation of PTX resistance in OC [24]. However, its speci c function and mechanism in OC have not been studied.…”

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confidence: 80%

PRPF6 promotes metastasis and paclitaxel resistance of ovarian cancer via SNHG16/CEBPB/GATA3 axis

Wang

Zhou

et al. 2022

Preprint

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Background: Metastasis and paclitaxel (PTX) resistance are the main reason for the poor prognosis of ovarian cancer (OC). Evidence has shown that RNA-binding proteins (RBPs) and long noncoding RNAs (lncRNAs) can modulate post-transcriptional regulation. The aim of this study was to determine the relationship among RBP, lncRNA and OC and to further guide clinical therapy. Methods: The expression of pre‐mRNA processing factor 6 (PRPF6) in OC tissues form 68 patients were detected by Immunohistochemistry. The expression of small nucleolar RNA host gene 16(SNHG16) transcripts-SNHG16-L/S in OC cell lines were analyzed by real-time PCR (RT-PCR). Transwell, CCK8 assays and flow cytometry analyses were used to detected effects of PRPF6 and SNHG16 on tumorigenesis and PTX-resistance. Molecular interactions were examined by dual‐luciferase reporter gene assay, RNA immunoprecipitation and chromatin immunoprecipitation. OC cells that knockdown PRPF6 were injected subcutaneously in nude mice.Results: The results showed that PRPF6 was upregulated in OC chemoresistant tissues and was closely related to advanced FIGO stages. PRPF6 promoted progression, and PTX resistance in vitro and in vivo. SNHG16-L/S were differentially expressed in OC cells and tissues as detected through real-time PCR (RT-PCR). SNHG16-L/S had opposite effects on progression and PTX resistance in OC. Mechanistically, SNHG16-L inhibited GATA-binding protein 3 (GATA3) transcription by binding to CCAAT/enhancer-binding protein B (CEBPB). Moreover, PRPF6 induced the alternative splicing of SNHG16, causing downregulation of SNHG16-L and, leading to the upregulation of GATA3 expression to further promote metastasis and PTX-resistance in OC.Conclusions: Totally, these data unveiled that PRPF6 promotes metastasis and PTX resistance of OC through SNHG16-L/CEBPB/GATA3 axis, which provides a new direction for OC treatment.

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Hybrid-polymerase chain reaction to identify novel target genes of miR-134 in paclitaxel resistant human ovarian carcinoma cells

Cited by 9 publications

References 35 publications

A novel p53 regulator, C16ORF72/TAPR1, buffers against telomerase inhibition

A novel p53 regulator, C16ORF72/TAPR1, buffers against telomerase inhibition

miR-134: A Human Cancer Suppressor?

PRPF6 promotes metastasis and paclitaxel resistance of ovarian cancer via SNHG16/CEBPB/GATA3 axis

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