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Knockdown of UCA1 restrains cell proliferation and metastasis of diffuse large B-cell lymphoma by counteracting miR-331-3p expression.

ABSTRACT: Long non-coding RNA urothelial cancer associated 1 (UCA1) has been reported to act as a carcinogen in bladder cancer, while its role in diffuse large B-cell lymphoma (DLBCL) remains unclear. The present study was designed to explore the expression pattern and role of UCA1 in DLBCL. The expression pattern of UCA1 and microRNA (miR)-331-3p in DLBCL tissues and cell lines were detected by RT-qPCR. Dual luciferase reporter assay was performed to explore the relationship between UCA1 and miR-331-3p. Cell proliferation was explored by MTT assay. Cell migration and invasion abilities were assessed by Transwell assay. In the present study, it was revealed that the expression of UCA1 was significantly upregulated, while miR-331-3p was downregulated in DLBCL tissues and cell lines. Moreover, UCA1 was revealed to competitively bind with miR-331-3p in DLBCL. Functionally, knockdown of UCA1 was revealed to suppress cell proliferation, migration and invasion in DLBCL cells. Furthermore, upregulation of miR-331-3p prevented cell proliferation, migration and invasion in DLBC cells. In conclusion, the present findings firstly demonstrated that UCA1 silencing restrained DLBCL cell proliferation and metastases viability by suppressing miR-331-3p expression. It is suggested that UCA1 could be a possible medicinal target and biomarker for DLBCL.

SUBMITTER: Zhang M

PROVIDER: S-EPMC7693482 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

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Knockdown of UCA1 restrains cell proliferation and metastasis of diffuse large B-cell lymphoma by counteracting miR-331-3p expression.

Zhang Minqing M Du Yiping Y Shang Jingmei J Zhang Dongqing D Dong Xiaoqing X Chen Hong H

Oncology letters 20201113 1

Long non-coding RNA urothelial cancer associated 1 (UCA1) has been reported to act as a carcinogen in bladder cancer, while its role in diffuse large B-cell lymphoma (DLBCL) remains unclear. The present study was designed to explore the expression pattern and role of UCA1 in DLBCL. The expression pattern of UCA1 and microRNA (miR)-331-3p in DLBCL tissues and cell lines were detected by RT-qPCR. Dual luciferase reporter assay was performed to explore the relationship between UCA1 and miR-331-3p. ...[more]

PMID: 33262831

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Project description:Objective:Mounting research has established the role of microRNAs (miRNAs) as oncogenes or anti-oncogenes (tumor suppressors) in the development and progression of several cancers. The purpose of our current study is to delineate the roles and functional mechanisms of miR-331-3p and MLLT10 in non-small cell lung cancer (NSCLC) tumorigenesis. Patients and Methods:Quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was employed to measure miR-331-3p expression levels in twenty-six matched tumor tissues and non-cancerous tissues collected from patients suffering from NSCLC, and from six NSCLC cell lines separately: A549, H1650, H292, H1299, H1944 and BEAS-2b. We employed the dual-luciferase activity assay to check whether the putative gene, MLLT10, was a downstream target of miR-331-3p in NSCLC pathogenesis and development. Western blot was conducted to analyze the protein expression levels of MLLT10 (AF10), E-cadherin, Vimentin, and GAPDH. CCK-8 assay, transwell migration assay, and transwell invasion assay were carried out to observe the functions of miR-331-3p and MLLT10 on NSCLC tumor cell proliferation, metastasis, and invasion, respectively. To identify whether the metastasis of NSCLC tumor cells was EMT-mediated, supplementary experiments involving E-cadherin and Vimentin were implemented. Results:miR-331-3p was downregulated in NSCLC, which promoted tumor cell proliferation, whereas the overexpression of miR-331-3p inhibited tumor cell proliferation. Being a direct target of miR-331-3p, MLLT10 was negatively modulated by miR-331-3p, which suppressed tumor cell proliferation, migration, and invasion in NSCLC. However, MLLT10 overexpression alleviated the above inhibitory effects. Furthermore, EMT-mediated metastasis was proved to be present in NSCLC. Conclusion:miR-331-3p played a suppressor role in NSCLC tumor cell proliferation, EMT-mediated metastasis, and invasion by targeting MLLT10. Our findings highlighted that miR-331-3p/MLLT10 axis could be useful as a clinical diagnostic marker and therapeutic target in NSCLC patients.

Project description:PURPOSE:Triple-negative breast cancer is characterized by fast progression with high possible for metastasis and poor survival. Dysfunction of microRNAs plays an important role in the initiation and progression of cancer. Our previous microRNA-seq data indicated the downregulation of miR-331-3p in triple-negative breast cancer tissues compared with that of the noncancer tissues. However, the function of miR-331-3p in triple-negative breast cancer remains largely unknown. Herein, the involvement of miR-331-3p in triple-negative breast cancer was investigated and the therapeutic potential of miR-331-3p was also explored. METHODS:Real-time quantitative polymerase chain reaction was performed to detect the expression of miR-331-3p in triple-negative breast cancer tissues and cell lines. The cell proliferation was determined by the cell counting kit-8 assay. Apoptosis of triple-negative breast cancer cells was examined by annexin V/propidium iodide staining. miRDB database was used to predict the potential targets of miR-331-3p. Western blot was performed to examine the expression of the target protein. RESULTS:miR-331-3p was significantly downregulated in triple-negative breast cancer tissues and cell line. Lower miR-331-3p expression was significantly correlated with the tumor size, TNM stage, and lymph node metastasis of patients with triple-negative breast cancer. Functional experiments showed that the overexpression of miR-331-3p inhibited the proliferation and increased apoptosis of triple-negative breast cancer cells. Neuropilin-2 was identified as a target of miR-331-3p, which harbored binding site of miR-331-3p in its 3'-untranslated region. Overexpression of miR-331-3p decreased the messenger RNA and protein levels of neuropilin-2 in triple-negative breast cancer cells. Restoration of neuropilin-2 partially reversed the inhibitory effects of miR-331-3p on the proliferation of triple-negative breast cancer cells. CONCLUSIONS:Our results demonstrated the novel function of miR-331-3p/neuropilin-2 signaling in regulating the malignant behaviors of triple-negative breast cancer cells, which suggested miR-331-3p as a potential target for the treatment of triple-negative breast cancer.

Dataset Information

Knockdown of UCA1 restrains cell proliferation and metastasis of diffuse large B-cell lymphoma by counteracting miR-331-3p expression.

Publications

Knockdown of UCA1 restrains cell proliferation and metastasis of diffuse large B-cell lymphoma by counteracting miR-331-3p expression.

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