MYBL2-induced PITPNA-AS1 upregulates SIK2 to exert oncogenic function in triple-negative breast cancer through miR-520d-5p and DDX54

Liu, Bolong; Yao, Pingbo; Xiao, Feng; Guo, Jiajie; Wu, Lianghui; Yong, Yang

doi:10.1186/s12967-021-02956-6

Cited by 13 publications

(9 citation statements)

References 35 publications

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“…lncRNAs have received a lot of attention in recent years, and they have played a pivotal role in various malignancies, notably LUSC. [10][11][12][13][14] PITPNA-AS1 is a novel lncRNA that has been investigated in LUSC to accelerate tumorigenesis. 16 However, the ceRNA regulation mechanism mediated by PITPNA-AS1 in LUSC is unknown.…”

Section: Discussionmentioning

confidence: 99%

“…LncRNA PITPNA antisense RNA 1 (PITPNA‐AS1) has been identified as a new lncRNA that has a role in the progression of a variety of malignancies. In triple‐negative breast cancer, PITPNA‐AS1 has been shown to have an oncogenic role by targeting the miR‐520d‐5p/DDX54 axis 14 . PITPNA‐AS1 also absorbs miR‐129‐5p to control UNC5B and accelerates papillary thyroid tumorigenesis 15 .…”

Section: Introductionmentioning

confidence: 99%

“…In triple-negative breast cancer, PITPNA-AS1 has been shown to have an oncogenic role by targeting the miR-520d-5p/DDX54 axis. 14 PITPNA-AS1 also absorbs miR-129-5p to control UNC5B and accelerates papillary thyroid tumorigenesis. 15 We found that PITPNA-AS1 has a higher expression level and exacerbates LUSC cell proliferation and migration through interacting with TAF15 to stabilize HMGB3.…”

Section: Introductionmentioning

confidence: 99%

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LncRNA PITPNA‐AS1/miR‐223‐3p/PTN axis regulates malignant progression and stemness in lung squamous cell carcinoma

Peng

Qiu

2022

Clinical Laboratory Analysis

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Background: Long noncoding RNAs (lncRNAs) are a kind of molecule that cannot code proteins, and their expression is dysregulated in diversified cancers. LncRNA PITPNA-AS1 has been shown to act as a tumor promoter in a variety of malignancies, but its function and regulatory mechanisms in lung squamous cell carcinoma (LUSC) are yet unknown. Methods:The mRNA and protein expression of genes were examined by RT-qPCR, western blot, and IHC assay. The cell proliferation, migration, invasion, and stemness were detected through CCK-8, colony formation, Transwell and spheroid formation assays. The CD44 + and CD166 + -positive cells were detected through flow cytometry.The binding ability among genes through luciferase reporter and RNA pull-down assays. The tumor growth was detected through in vivo nude mice assay. Results:The lncRNA PITPNA-AS1 had increased expression in LUSC and was linked to a poor prognosis. In LUSC, PITPNA-AS1 also enhanced cell proliferation, migration, invasion, and stemness. This mechanistic investigation showed that PITPNA-AS1 absorbed miR-223-3p and that miR-223-3p targeted PTN. MiR-223-3p inhibition or PTN overexpression might reverse the inhibitory effects of PITPNA-AS1 suppression on LUSC progression, as demonstrated by rescue experiments. In addition, the PITPNA-AS1/miR-223-3p/PTN axis accelerated tumor development in vivo. Conclusions: It is the first time we investigated the potential role and ceRNA regulatory mechanism of PITPNA-AS1 in LUSC. The data disclosed that PITPNA-AS1 upregulated PTN through sponging miR-223-3p to enhance the onset and progression of LUSC. These findings suggested the ceRNA axis may serve as a promising therapeutic biomarker for LUSC patients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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LncRNA PITPNA‐AS1/miR‐223‐3p/PTN axis regulates malignant progression and stemness in lung squamous cell carcinoma

Peng

Qiu

2022

Clinical Laboratory Analysis

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“…Likewise, our studies showed that LINC01608 was overexpressed in HCC and functioned as a ceRNA for miR‐875‐5p to promote HCC progression. Additionally, recent studies had demonstrated that some transcriptional factors, such as SP1 and MYBL2, could combine with the promoter of LncRNAs and regulate their expression 24,25 . YY1 is a transcriptional factor ubiquitously expressed in mammalian cells.…”

Section: Discussionmentioning

confidence: 99%

LINC01608 activated by YY1 facilitate hepatocellular carcinoma progression by modulating the EGFR/ERK axis

Han

Liu

et al. 2022

Liver International

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Background: Long non-coding RNAs (LncRNAs) have been demonstrated to associate with a variety of cancers. However, the mechanisms of LncRNAs in hepatocellular carcinoma (HCC) progression are still not fully clarified.Methods: LINC01608 expression level in HCC and adjacent normal tissues was detected by real-time-quantitively PCR (RT-qPCR) in clinical samples and in situ hybridization (ISH) in tissue microarray. Several functional assays were performed to determine the biological effects of LINC01608 in HCC cells in vitro, while subcutaneous xenograft models and lung metastasis models in nude mice and immunohistochemistry (IHC) results showed the role of LINC01608 in HCC progression in vivo.The combination of LINC01608 with miR-875-5p and target genes was elucidated by dual-luciferase report assays, RNA immunoprecipitation (RIP) assays and fluorescence in situ hybridization (FISH) assays. Finally, bioinformatics analysis and chromatin immunoprecipitation (CHIP) were performed to investigate the mechanism of Yin Yang-1 (YY1) regulating LINC01608 transcription.Results: LINC01608 was overexpressed in HCC tissues, and high LINC01608 expression predicted poor overall survival (OS) and disease-free survival (DFS) in HCC patients. LINC01608 could promote HCC cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro and in vivo. Furthermore, we demonstrated that LINC01608 could sponge to miR-875-5p and activate the EGFR/ERK pathway. Moreover, we identified transcriptional factor YY1 could bind to the promoter of LINC01608 and induce its transcription. Conclusion:LINC01608 could serve as a promising prognostic biomarker of HCC. YY1-activated LINC01608 could promote HCC progression by associating with miR-875-5p to induce the EGFR/ERK signalling pathway. This discovery might provide therapeutic strategies for HCC.

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“…A large body of literature has found that MYBL2 overexpression plays an oncogenic role in cancers, such as colorectal cancer and hepatocellular carcinoma [ 12 , 13 ]. MYBL2-induced PITPNA antisense RNA 1 (PITPNA-AS1) upregulates salt-inducible kinase 2 (SIK2) to exert oncogenic functions in triple-negative breast cancer [ 14 ]. Besides, MYBL2 was reported to play important regulatory roles in proliferation, differentiation, and cell cycle [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Actin-binding Rho activating C-terminal like (ABRACL) transcriptionally regulated by MYB proto-oncogene like 2 (MYBL2) promotes the proliferation, invasion, migration and epithelial-mesenchymal transition of breast cancer cells

Chen

2022

Bioengineered

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Breast cancer is the most common malignant tumor in females with high incidence and mortality. Actin-binding Rho activating C-terminal like (ABRACL) was highly expressed in several cancers. We aimed to investigate the function and mechanism of ABRACL in breast cancer. In this study, biological information analysis predicted the expression of ABRACL and MYB proto-oncogene-like 2 (MYBL2) in breast cancer tissues and their possible relationship. With the application of RT-qPCR and western blot, the mRNA and protein expression of ABRACL and MYBL2 in breast cancer cell lines were assessed. After ABRACL interference, an assessment of cell proliferation was carried out using cell counting kit (CCK)-8, colony formation, and western blot. The invasive and migratory abilities of cells were determined by transwell and wound healing assays. The epithelial-mesenchymal transition (EMT) process was assayed utilizing western blot. The relationship between ABRACL and MYBL2 was confirmed by luciferase reporter assay and chromatin immunoprecipitation (ChIP). The above experiments were done again after MYBL2 overexpression in breast cancer cells with ABRACL deletion. Results revealed that ABRACL and MYBL2 were highly expressed in breast cancer tissues and cells. ABRACL knockdown suppressed the proliferation, invasion, migration, and EMT of breast cancer cells. MYBL2 transcriptionally activated ABRACL. Besides, MYBL2 overexpression reversed the effects of ABRACL knockdown on cell malignant biological behaviors. To conclude, ABRACL could be transcriptionally regulated by MYBL2 to promote cell malignant biological behaviors in breast cancer cells, implying the potential of ABRACL being a promising target for the improvement of breast cancer therapy.

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MYBL2-induced PITPNA-AS1 upregulates SIK2 to exert oncogenic function in triple-negative breast cancer through miR-520d-5p and DDX54

Cited by 13 publications

References 35 publications

LncRNA PITPNA‐AS1/miR‐223‐3p/PTN axis regulates malignant progression and stemness in lung squamous cell carcinoma

LncRNA PITPNA‐AS1/miR‐223‐3p/PTN axis regulates malignant progression and stemness in lung squamous cell carcinoma

LINC01608 activated by YY1 facilitate hepatocellular carcinoma progression by modulating the EGFR/ERK axis

Actin-binding Rho activating C-terminal like (ABRACL) transcriptionally regulated by MYB proto-oncogene like 2 (MYBL2) promotes the proliferation, invasion, migration and epithelial-mesenchymal transition of breast cancer cells

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