The Functional Role of LncRNA UCA1 in Pancreatic Cancer: a mini-review

Sun, Cen-Cen; Li, Li; jiang, Zhi-Chen; Liu, Zhengchuang; Wang, Liang; Wang, Hui-Ju

doi:10.7150/jca.79171

Cited by 5 publications

(2 citation statements)

References 83 publications

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“… 15 LncRNAs are involved in several physiological processes because they regulate gene expression at the epigenetic, transcriptional, and post-transcriptional levels. 16 Aberrant expression is also closely associated with tumor proliferation, differentiation, apoptosis, and metastasis. 17 The lncRNA MIR4435-2 host gene (MIR4435-2HG) is located on human chromosome 2q13.…”

Section: Introductionmentioning

confidence: 99%

M2 Macrophage-Derived Exosomal lncRNA MIR4435-2HG Promotes Progression of Infantile Hemangiomas by Targeting HNRNPA1

Li,

Cao,

et al. 2023

IJN

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Purpose Infantile hemangiomas (IHs) are commonly observed benign tumors that can cause serious complications. M2-polarized macrophages in IHs promote disease progression. In this study, we investigated the role of M2 macrophage-derived exosomal lncRNA MIR4435-2HG in IHs. Patients and Methods Exosomes derived from M2 polarized macrophages were extracted. Next, using cell co-culture or transfection, we investigated whether M2 polarized macrophage-derived exosomes (M2-exos) can transport MIR4435-2HG to regulate the proliferation, migration, invasion, and angiogenesis of hemangioma-derived endothelial cells (HemECs). RNA-seq and RNA pull-down assays were performed to identify targets and regulatory pathways of MIR4435-2HG. We explored the possible mechanisms through which MIR4435-2HG regulates the biological function of HemECs. Results M2-exos significantly enhanced the proliferation, migration, invasion, and angiogenesis of HemECs. Thus, HemECs uptake M2-exos and promote biological functions through the inclusion of MIR4435-2HG. RNA-seq and RNA pull-down experiments confirmed that MIR4435-2HG regulates of HNRNPA1 expression and directly binds to HNRNPA1, consequently affecting the NF-κB signal pathway. Conclusion MIR4435-2HG of M2-exos promotes the progression of IHs and enhances the proliferation, migration, invasion, and angiogenesis of HemECs by directly binding to HNRNPA1. This study not only reveals the mechanism of interaction between M2 macrophages and HemECs, but also provides a promising therapeutic target for IHs.

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Section: Introductionmentioning

confidence: 99%

M2 Macrophage-Derived Exosomal lncRNA MIR4435-2HG Promotes Progression of Infantile Hemangiomas by Targeting HNRNPA1

Li,

Cao,

et al. 2023

IJN

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“…Recently, Sun et al. reviewed the functions and pointed out the importance of UCA1 in pancreatic cancer, who showed that UCA1 contributed to carcinogenesis, angiogenesis, and drug resistance via several signal pathways ( 13 ). Despite this, few details about UCA1 in pancreatic cancer are known, the regulatory role and mechanism of UCA1 are still unclear.…”

Section: Introductionmentioning

confidence: 99%

UCA1 executes an oncogenic role in pancreatic cancer by regulating miR-582-5p/BRCC3

2023

Front. Oncol.

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BackgroundAs a fatal disease, the mechanism of pancreatic cancer is unclear. Urothelial carcinoma antigen 1(UCA1), a long noncoding RNA (lncRNA) that was first reported in bladder cancer, acts as an oncogene. However, the regulatory role and mechanism of UCA1 in pancreatic cancer remain unknown. This study aims to investigate the expression level and prognostic value of UCA1 in pancreatic cancer tissues, the effects and mechanism of UCA1 in regulating cell proliferation, apoptosis and metastasis.MethodsUCA1 expression levels in tissues were detected by in situ hybridization (ISH) and the prognostic value was evaluated by univariate and multivariate survival analysis. For in vitro experiments, proliferation was evaluated by a cell count kit assay, Edu experiments, and a clone formation assay. Apoptosis was evaluated by fluorescence-activated cell sorting flow-cytometry. Cell migration and invasion capacities were detected by wound healing and transwell assays. Western blots were performed to detect apoptotic associated molecules and epithelial-mesenchymal transition (EMT) markers. For the in vivo experiment, subcutaneous transplantation models of pancreatic cancer in nude mice were established to observe the tumor growth. The regulatory mechanism of UCA1 was explored by proteomics, bioinformatic analysis, luciferase reporter assays, and rescue experiments.ResultsISH staining revealed that UCA1 levels between cancer tissues (n=94) and tumor-adjacent tissues (n=73) did not show significant differences. Survival analysis indicated that high expression of UCA1 was an unfavorable prognosis factor for pancreatic cancer. Downregulation of UCA1 by siRNA significantly inhibited cell proliferation, decreased the capacities of cell migration and invasion, induced cell apoptosis, and inhibited EMT. Furthermore, we demonstrated that UCA1 positively regulated the expression of BRCC3 by inhibiting miR-582-5p. Rescue experiments indicated that either inhibiting the expression of miR-582-5p or enhancing expression of BRCC3 could partly attenuate the antitumor effects of downregulation of UCA1.ConclusionUCA1 acted as an oncogene in pancreatic cancer by partly regulating miR-582-5p/BRCC3, which could be a new therapeutic target for pancreatic cancer.

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Silencing of lncRNA UCA1 Reverses Doxorubicin Resistance of Breast Cancer Through Inhibiting PI3K/AKT/mTOR Signaling Pathway

Suicmez,

Namalir,

Konus

et al. 2024

ChemistrySelect

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The role of silencing of long non coding RNA UCA1 gene in the development of resistance to doxorubicin in breast cancer was employed. We initially induced resistance to doxorubicin in MCF‐7 cells, reaching a level of 0.64 μM. Next, we employed the cytotoxicity test to assess the progression of doxorubicin resistance in both sensitive cells (MCF‐7/S) and the resistant cells (MCF‐7/Dox). IC50 values of MCF‐7/S and MCF‐7/Dox were determined as 1.65 μM and 128.5 μM, respectively. Then, UCA1 siRNA was transfected to MCF‐7/Dox and MCF‐7/S cells by lipofectamine method. After that, the expression levels of AKT1, PTEN, AKT2 and mTOR genes, which are involved in the PI3K/AKT/mTOR signaling pathway, were analyzed by qPCR. Finally, it was determined that the mRNA level of the UCA1 gene suppressed by siRNA was significantly decreased in MCF‐7/S and MCF‐7/Dox cells, except PTEN, compared to the control groups. These results emphasized that silencing of lncRNA UCA1 gene negatively regulates cell growth, differentiation and proliferation.

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The Functional Role of LncRNA UCA1 in Pancreatic Cancer: a mini-review

Cited by 5 publications

References 83 publications

M2 Macrophage-Derived Exosomal lncRNA MIR4435-2HG Promotes Progression of Infantile Hemangiomas by Targeting HNRNPA1

M2 Macrophage-Derived Exosomal lncRNA MIR4435-2HG Promotes Progression of Infantile Hemangiomas by Targeting HNRNPA1

UCA1 executes an oncogenic role in pancreatic cancer by regulating miR-582-5p/BRCC3

Silencing of lncRNA UCA1 Reverses Doxorubicin Resistance of Breast Cancer Through Inhibiting PI3K/AKT/mTOR Signaling Pathway

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