LncRNA terminal differentiation-induced ncRNA (TINCR) sponges miR-302 to upregulate cyclin D1 in cervical squamous cell carcinoma (CSCC)

Hou, Anli; Zhang, Yali; Zheng, Yi; Fan, Yonggang; Liu, Huilan; Zhou, Xifa

doi:10.1007/s13577-019-00268-y

Cited by 14 publications

(8 citation statements)

References 18 publications

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“…Increased TINCR lncRNA levels have been found within differentiated superficial epidermis layers and were shown to positively regulate the expression of the MAF:MAFB TF dimer (52). Corroborating our findings, higher expression of TINCR in cervical SCC was previously observed (53), although these data contrast with data obtained from TCGA (54). All other validated lncRNA genes in our study were classified as antisense transcripts (55).…”

Section: Epithelium Structure and Function Pathways Are Enriched In Cervical Squamous Cell Carcinoma Gene Profilesupporting

confidence: 76%

Dysregulation of Transcription Factor Networks Unveils Different Pathways in Human Papillomavirus 16-Positive Squamous Cell Carcinoma and Adenocarcinoma of the Uterine Cervix

et al. 2021

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Squamous cell carcinoma (SCC) and adenocarcinoma (ADC) are the most common histological types of cervical cancer (CC). The worse prognosis of ADC cases highlights the need for better molecular characterization regarding differences between these CC types. RNA-Seq analysis of seven SCC and three ADC human papillomavirus 16-positive samples and the comparison with public data from non-tumoral human papillomavirus-negative cervical tissue samples revealed pathways exclusive to each histological type, such as the epithelial maintenance in SCC and the maturity-onset diabetes of the young (MODY) pathway in ADC. The transcriptional regulatory network analysis of cervical SCC samples unveiled a set of six transcription factor (TF) genes with the potential to positively regulate long non-coding RNA genes DSG1-AS1, CALML3-AS1, IGFL2-AS1, and TINCR. Additional analysis revealed a set of MODY TFs regulated in the sequence predicted to be repressed by miR-96-5p or miR-28-3p in ADC. These microRNAs were previously described to target LINC02381, which was predicted to be positively regulated by two MODY TFs upregulated in cervical ADC. Therefore, we hypothesize LINC02381 might act by decreasing the levels of miR-96-5p and miR-28-3p, promoting the MODY activation in cervical ADC. The novel TF networks here described should be explored for the development of more efficient diagnostic tools.

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Section: Epithelium Structure and Function Pathways Are Enriched In Cervical Squamous Cell Carcinoma Gene Profilesupporting

confidence: 76%

Dysregulation of Transcription Factor Networks Unveils Different Pathways in Human Papillomavirus 16-Positive Squamous Cell Carcinoma and Adenocarcinoma of the Uterine Cervix

et al. 2021

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“…Additionally, TINCR can serve as a competing endogenous RNA by sponging miR-375, and promote proliferation and inhibit apoptosis 27 . The high expression of TINCR and its carcinogenic effect were also observed in epithelial ovarian cancer 28 , breast cancer 18 , cervical squamous cell carcinoma 29 , hepatocellular carcinoma 30 , non-small cell lung cancer 31 , nasopharyngeal carcinoma 32 , and bladder urothelial carcinoma 33 , which suggests that TINCR may be a strategic target for cancer treatment. However, the opposite situation was found in lung adenocarcinoma 34 , colorectal cancer 35 , prostate cancer 36 , melanoma 37 , oral squamous cell carcinoma 38 , and skin cancer 39 , with a down-regulation in these cancers.…”

Section: Discussionmentioning

confidence: 91%

Genetic predisposition to papillary thyroid carcinoma is mediated by a long non-coding RNA TINCR enhancer polymorphism

Wang

Huang

Chen

et al. 2021

Preprint

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Single nucleotide polymorphisms (SNPs) in the enhancer region have been demonstrated to confer to altered enhancer activities, aberrant gene expression, and cancer susceptibility. In this study, we aimed to examine the association between an SNP, rs8101923, within terminal differentiation-induced non-coding RNA (TINCR) and the risk of papillary thyroid carcinoma (PTC). Blood samples from 559 patients with PTC and 445 healthy individuals were collected. The rs8101923 was genotyped by using polymerase chain reaction-restriction fragment length polymorphism assay. The impact of the rs8101923 on TINCR expression and enhancer activity was evaluated by quantitative real-time PCR and dual-luciferase reporter assay. The binding of AP-2α to TINCR enhancer was determined by chromatin immunoprecipitation. The rs8101923 G allele was significantly associated with a higher risk of PTC (adjusted OR = 1.37; 95% CI: 1.15–1.64). Mechanistically, the rs8101923 was related to increased transcriptional levels and enhancer activities (P < 0.05). Transcription factor AP-2α binds to the enhancer region of TINCR containing the rs8101923 locus, and promotes cell proliferation in PTC. These findings suggest the rs8101923 as a risk factor in the pathogenesis of PTC, which provides evidence for explaining the mechanism of the rs8101923 risk allele predisposing to PTC.

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“…Moreover, miR-215-3p is reported to play a negative role in cell growth, migration and invasion of CRC by interacting with its target FOXM1 (10). miR-302e is one of the 8 members of the miR-302 family able to suppress the proliferation of cervical squamous cell carcinoma and breast cancer, also to impede the angiogenesis and cell invasion of CRC (29)(30)(31). To make the functional mechanism of CXCL1 in CRC more specific, this study firstly used bioinformatics methods and identified that CXCL1 was a downstream target of miR-302e.…”

Section: Discussionmentioning

confidence: 99%

CXCL1 Regulated by miR-302e Is Involved in Cell Viability and Motility of Colorectal Cancer via Inhibiting JAK-STAT Signaling Pathway

et al. 2021

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PurposeThis study made a systemic description for the CXCL1-dependent regulatory mechanism in colorectal cancer (CRC).MethodsBioinformatics methods were applied to obtain target mRNA CXCL1 and corresponding upstream miRNA. qRT-PCR and Western blot were performed to measure the levels of CXCL1 and miR-302e in CRC tissue and cells. Experiments including CCK-8, wound healing assay, Transwell invasion assay, and flow cytometry were conducted to assess cell biological behaviors. Dual-luciferase reporter assay was carried out for verification of the targeting relationship between CXCL1 and miR-302e. The inhibitor AG490 of JAK-STAT signaling pathway was used to identify the functional mechanism of CXCL1/JAK-STAT underlying progression of CRC, and tumor xenograft experiments were performed for further validation.ResultsCXCL1 was highly expressed in CRC tissue and cells, while miR-302e was poorly expressed. Silencing CXCL1 or overexpressing miR-302e could lead to inhibition of cell proliferation, migration, invasion but promotion of cell apoptosis of CRC. Besides, CXCL1 was identified as a direct target of miR-302e, and CXCL1 could reverse the effect of miR-302e on cell proliferation, migration, invasion, and apoptosis. Furthermore, CXCL1 functioned on CRC cell biological behaviors via activation of JAK-STAT signaling pathway.ConclusionCXCL1 could be regulated by miR-302e to inactivate JAK-STAT signaling pathway, in turn affecting cell proliferation, migration, invasion, and apoptosis of CRC. Our result provides a potential therapeutic target for CRC treatment.

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LncRNA terminal differentiation-induced ncRNA (TINCR) sponges miR-302 to upregulate cyclin D1 in cervical squamous cell carcinoma (CSCC)

Cited by 14 publications

References 18 publications

Dysregulation of Transcription Factor Networks Unveils Different Pathways in Human Papillomavirus 16-Positive Squamous Cell Carcinoma and Adenocarcinoma of the Uterine Cervix

Dysregulation of Transcription Factor Networks Unveils Different Pathways in Human Papillomavirus 16-Positive Squamous Cell Carcinoma and Adenocarcinoma of the Uterine Cervix

Genetic predisposition to papillary thyroid carcinoma is mediated by a long non-coding RNA TINCR enhancer polymorphism

CXCL1 Regulated by miR-302e Is Involved in Cell Viability and Motility of Colorectal Cancer via Inhibiting JAK-STAT Signaling Pathway

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