Study of the biological function of LncRNA LUCAT1 on cervical cancer cells by targeting miR-199b-5p

Yang, Ting; Xia, Shengnan

doi:10.1042/bsr20200422

Cited by 11 publications

(7 citation statements)

References 24 publications

(24 reference statements)

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“…After knocking out LUCAT1, CRC cell proliferation was significantly inhibited. This is also consistent with the results of studies in cervical cancer, ovarian cancer, breast cancer, choroidal melanoma, clear cell renal cell carcinoma, non-small-cell lung cancer and esophageal squamous cell carcinoma, showing that loss of LUCAT1 hinders cell proliferation 15,17,20,39,[41][42][43] . The results described above indicate the oncogenic role of LUCAT1 in CRC.…”

Section: Discussionsupporting

confidence: 90%

“…In addition, a systematic analysis of online databases in our study discovered that LUCAT1 could be a risk factor for prognosis in CRC patients, suggesting it might be a potential therapeutic target for CRC. Similar condition is reported in cervical cancer 39 and non-small-cell lung cancer 15 , showing that highly expressed LUCAT1 in peripheral blood or tissue of patients is related to poorer survival. To further investigate the oncogenic role of LUCAT1 in CRC, we transfected the CRISPR/Cas9 system with dual sgRNAs into HCT116 and SW620 cells to knock out the full-length LUCAT1 gene coding sequence.…”

Section: Discussionsupporting

confidence: 78%

“…In addition, LUCAT1 has been reported to induce CRC cell cycle arrest and apoptosis by binding to UBA52 and activating the p53 pathway 44 . Some studies also explore the relationship between LUCAT1 and miRNAs, including miR-514a/b-3b in choroidal melanoma, miR-199a-5p in ovarian cancer, and miR-199b-5p in cervical cancer 39,41,42 . LUCAT1 are found to share conserved binding site with these miRNAs and then modulates cancer progression through their direct interaction.…”

Section: Discussionmentioning

confidence: 99%

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The long noncoding RNA LUCAT1 promotes colorectal cancer cell proliferation by antagonizing Nucleolin to regulate MYC expression

Bai

et al. 2020

Cell Death Dis

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The long noncoding RNA (lncRNA) LUCAT1 was recently reported to be upregulated and to play an essential role in multiple cancer types, especially colorectal cancer (CRC), but the molecular mechanisms of LUCAT1 in CRC are mostly unreported. Here, a systematic analysis of LUACT1 expression is performed with data from TCGA database and clinic CRC samples. LUCAT1 is identified as a putative oncogene, which is significantly upregulated in CRC and is associated with poor prognosis. Loss of LUCAT1 restricts CRC proliferative capacities in vitro and in vivo. Mechanically, NCL is identified as the protein binding partner of LUCAT1 by using chromatin isolation by RNA purification coupled with mass spectrometry (ChIRP-MS) and RNA immunoprecipitation assays. We also show that NCL directly binds to LUCAT1 via its putative G-quadruplex-forming regions from nucleotides 717 to 746. The interaction between LUCAT1 and NCL interferes NCL-mediated inhibition of MYC and promote the expression of MYC. Cells lacking LUCAT1 show a decreased MYC expression, and NCL knockdown rescue LUCAT1 depletion-induced inhibition of CRC cell proliferation and MYC expression. Our results suggest that LUCAT1 plays a critical role in CRC cell proliferation by inhibiting the function of NCL via its G-quadruplex structure and may serve as a new prognostic biomarker and effective therapeutic target for CRC.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

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The long noncoding RNA LUCAT1 promotes colorectal cancer cell proliferation by antagonizing Nucleolin to regulate MYC expression

Bai

et al. 2020

Cell Death Dis

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“…To further investigate the molecular mechanisms underlying the role of LUCAT1 in the tumorigenesis of LSCC, the ENCORI database ( ) was used. It was predicted that LUCAT1 directly bound with miR-493, a miRNA previously reported to inhibit tumorigenesis occurred in the 3′-UTR ( 29 , 30 ) ( Fig. 5A ).…”

Section: Resultsmentioning

confidence: 91%

Lung cancer‑associated transcript 1 facilitates tumorigenesis in laryngeal squamous cell carcinoma through the targeted inhibition of miR‑493

et al. 2020

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Long non-coding RNAs (lncRNAs) serve important roles in the tumorigenesis of a diverse range of cancer types. The lung cancer-associated transcript 1 (LUCAT1), has been reported to promote the proliferation, migration and invasion of oral squamous cell carcinoma cells. However, the exact role of LUCAT1 in laryngeal squamous cell carcinoma (LSCC) remains to fully understood. The present study aimed to interrogate the role and modulatory mechanism of LUCAT1 in LSCC. Reverse transcription-quantitative PCR and western blotting were used to investigate the expression of LUCAT1 and miR-493, as well as the protein expression of cyclin-dependent kinase 2, cyclin E1, p21, matrix metalloproteinase (MMP)2, MMP9, vascular endothelial growth factor-C, Bcl-2, Bax, cleaved caspase-3 and procaspase-3. Cell Counting Kit-8, flow cytometry, wound healing and Transwell assays were performed to analyze the proliferation, cell cycle, apoptosis levels, and the migratory and invasive abilities, respectively, of the LSCC AMC-HN-8 cell line. In addition, dual-luciferase reporter and ribonucleoprotein immunoprecipitation assays were used to investigate the binding between LUCAT1 and microRNA (miR)-493. The results of the present study revealed that the expression levels of LUCAT1 were upregulated in AMC-HN-8 cells. The genetic knockdown of LUCAT1 expression levels significantly suppressed the cell proliferation, alongside downregulating the expression levels of CDK2 and cyclin E1 and upregulating p21 expression levels. In addition, the knockdown of LUCAT1 inhibited cell migration and invasion, as demonstrated using the wound healing and Transwell assays, respectively. Moreover, LUCAT1 knockdown promoted cell apoptosis and upregulated the expression levels of Bax and cleaved caspase-3, whilst downregulating the expression levels of Bcl-2. Furthermore, LUCAT1 was discovered to directly bind to and inhibit the well-known tumor suppressor, miR-493. Notably, the specific inhibition of miR-493 partly blocked the anticancer effects of LUCAT1 knockdown in AMC-HN-8 cells. In conclusion, these results suggested that LUCAT1 may facilitate tumorigenesis in LSCC through the targeted inhibition of miR-493, which provides evidence for a novel target for the treatment of LSCC.

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“…Cervical cancer is one of the most common gynecological malignancies (57). The pathogenesis of cervical cancer is a complex process involving multiple factors and steps (58,59).…”

Section: Txnip and Cervical Cancermentioning

confidence: 99%

Research Progress of TXNIP as a Tumor Suppressor Gene Participating in the Metabolic Reprogramming and Oxidative Stress of Cancer Cells in Various Cancers

et al. 2020

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Thioredoxin-interacting protein (TXNIP) is a thioredoxin-binding protein that can mediate oxidative stress, inhibit cell proliferation, and induce apoptosis by inhibiting the function of the thioredoxin system. TXNIP is important because of its wide range of functions in cardiovascular diseases, neurodegenerative diseases, cancer, diabetes, and other diseases. Increasing evidence has shown that TXNIP expression is low in tumors and that it may act as a tumor suppressor in various cancer types such as hepatocarcinoma, breast cancer, and lung cancer. TXNIP is known to inhibit the proliferation of breast cancer cells by affecting metabolic reprogramming and can affect the invasion and migration of breast cancer cells through the TXNIP-HIF1α-TWIST signaling axis. TXNIP can also prevent the occurrence of bladder cancer by inhibiting the activation of ERK, which inhibits apoptosis in bladder cancer cells. In this review, we find that TXNIP can be regulated by binding to transcription factors or other binding proteins and can also be downregulated by epigenetic changes or miRNA. In addition, we also summarize emerging insights on TXNIP expression and its functional role in different kinds of cancers, as well as clarify its participation in metabolic reprogramming and oxidative stress in cancer cells, wherein it acts as a putative tumor suppressor gene to inhibit the proliferation, invasion, and migration of different tumor cells as well as promote apoptosis in these cells. TXNIP may therefore be of basic and clinical significance for finding novel molecular targets that can facilitate the diagnosis and treatment of malignant tumors.

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Study of the biological function of LncRNA LUCAT1 on cervical cancer cells by targeting miR-199b-5p

Cited by 11 publications

References 24 publications

The long noncoding RNA LUCAT1 promotes colorectal cancer cell proliferation by antagonizing Nucleolin to regulate MYC expression

The long noncoding RNA LUCAT1 promotes colorectal cancer cell proliferation by antagonizing Nucleolin to regulate MYC expression

Lung cancer‑associated transcript 1 facilitates tumorigenesis in laryngeal squamous cell carcinoma through the targeted inhibition of miR‑493

Research Progress of TXNIP as a Tumor Suppressor Gene Participating in the Metabolic Reprogramming and Oxidative Stress of Cancer Cells in Various Cancers

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