miR-361-3p Regulates Liver Tumor-initiating Cells Expansion and Chemo-resistance

Qu, Shen; Zhang, Xiaobing; Fan, Hengwei; Wu, Yue; Zhai, Jian; Wu, Dong

doi:10.21203/rs.3.rs-54212/v1

Cited by 4 publications

(4 citation statements)

References 34 publications

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“…MiR-361-3p expression is upregulated in HCC cells and liver tumorinitiating cells. The dysregulated expression of miR-361-3p enhances the self-renewal and tumorigenic liver tumor-initiating cells [25,26]. In agreement with findings from previous studies, we also observed a decrease in miR-361-3p expression in HCC tissues and cell lines.…”

Section: Discussionsupporting

confidence: 92%

Hsa_circ_0011385 knockdown represses cell proliferation in hepatocellular carcinoma

Yang

et al. 2021

Cell Death Discov.

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Circular RNAs (circRNAs), continuous loops of single-stranded RNA, regulate gene expression during the development of various cancers. However, the function of circRNAs in hepatocellular carcinoma (HCC) is rarely discussed. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the mRNA levels of circ_0011385, miR-361-3p, and STC2 in 96 pairs of HCC tissues (tumor tissues and adjacent normal tissues), HCC cell lines, and L02 (human normal liver cell line) cells. The relationships between circ_0011385 expression and clinical features of HCC were evaluated. Functional experiments in vitro or in vivo were used to evaluate the biological function of circ_0011385. Bioinformatics analysis was performed to predict miRNAs and mRNAs sponged by circ_0011385. RNA immunoprecipitation (RIP) and dual-luciferase reporter gene assays were used to elucidate the interactions among circ_0011385, miR-361-3p, and STC2 (stanniocalcin 2). ChIP and dual-luciferase reporter gene assays were used to identify the upstream regulator of circ_0011385. High expression of circ_0011385 was observed in HCC tissues and cell lines and was significantly associated with tumor size, TNM stage, and prognosis. In addition, inhibition of circ_0011385 expression prevented the proliferation of HCC cells in vitro and in vivo. Circ_0011385 sponged miR-361-3p, thereby regulating the mRNA expression of STC2. In addition, the transcription of circ_0011385 was regulated by SP3. Circ_0011385 knockdown suppressed cell proliferation and tumor activity in HCC. Circ_0011385 may therefore serve as a new biomarker in the diagnosis and treatment of HCC.

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Section: Discussionsupporting

confidence: 92%

Hsa_circ_0011385 knockdown represses cell proliferation in hepatocellular carcinoma

Yang

et al. 2021

Cell Death Discov.

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“…Compared with control cells, overexpression of miR-361-3p in HCC induced greater tumorigenicity and lower sensitivity to cisplatin through a mechanism that involves SOX1 binding. In addition, high levels of miR-361-3p in HCC patients treated with postoperative TACE were associated with shorter survival, 52 suggesting that this miRNA could be used as a prognostic biomarker.…”

Section: Mechanisms Of Pharmacoresistancementioning

confidence: 99%

Mechanisms of Pharmacoresistance in Hepatocellular Carcinoma: New Drugs but Old Problems

et al. 2021

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Hepatocellular carcinoma (HCC) is a malignancy with poor prognosis when diagnosed at advanced stages in which curative treatments are no longer applicable. A small group of these patients may still benefit from transarterial chemoembolization. The only therapeutic option for most patients with advanced HCC is systemic pharmacological treatments based on tyrosine kinase inhibitors (TKIs) and immunotherapy. Available drugs only slightly increase survival, as tumor cells possess additive and synergistic mechanisms of pharmacoresistance (MPRs) prior to or enhanced during treatment. Understanding the molecular basis of MPRs is crucial to elucidate the genetic signature underlying HCC resistome. This will permit the selection of biomarkers to predict drug treatment response and identify tumor weaknesses in a personalized and dynamic way. In this article, we have reviewed the role of MPRs in current first-line drugs and the combinations of immunotherapeutic agents with novel TKIs being tested in the treatment of advanced HCC.

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“…32 miR-361-3p has been rstly demonstrated as a novel oncogene. 23 Additional works continue to elucidate that miR-361-3p regulates the proliferation, migration, and invasion of human liver cancer, 33 prostate cancer cells, 21 and oral squamous cell carcinoma (OSCC). 20 For instance, miR-361-3p induced cell proliferation and promoted EMT through negative regulation of dual speci city phosphatase-2 (DUSP2), thereby activating ERK signaling in pancreatic cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Linoleic acid derivatives target miR-361-3p/BTG2 to confer anticancer effects in acute myeloid leukemia

Liu

et al. 2022

Preprint

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Acute myeloid leukemia (AML) is a deadly hematologic malignancy. Studies have shown that miroRNAs (miRNAs), evolutionarily conserved small noncoding RNAs, contribute to AML disease development, suggesting that therapeutical manipulation of miRNAs may benefit disease treatment in AML. In this study, we found miR-361-3p was significantly upregulated in the blood of AML patients, whereas the expression of its direct target, B-cell translocation gene (BTG2, a tumor suppressor), was markedly lower compared with the expression in the blood of healthy controls. Inhibition of miR-361-3p significantly increased BTG2, leading to inhibition of cell proliferation and promotion of cell apoptosis in AML cell line, HL-60. In contrast, increasing of miR-361-3p expression exerted opposite effects to miR-361-3p inhibitor on BTG2 expression, cell proliferation and apoptosis. We further showed 9s-Hydroxyoctadecadienoic acid (9s-HODE), a major active derivative of linoleic acid, exerted an anti-AML effect through, at least partly, targeting miR-361-3p/BTG2 axis and its associated pathways. These findings not just demonstrate an oncogenic role of miR-361-3p in AML but also provide novel insights to develop a potential therapeutic for AML treatment by manipulating its expressions.

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miR-361-3p Regulates Liver Tumor-initiating Cells Expansion and Chemo-resistance

Cited by 4 publications

References 34 publications

Hsa_circ_0011385 knockdown represses cell proliferation in hepatocellular carcinoma

Hsa_circ_0011385 knockdown represses cell proliferation in hepatocellular carcinoma

Mechanisms of Pharmacoresistance in Hepatocellular Carcinoma: New Drugs but Old Problems

Linoleic acid derivatives target miR-361-3p/BTG2 to confer anticancer effects in acute myeloid leukemia

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