LncRNA <i>TUG1</i> Promotes Hepatocellular Carcinoma Migration and Invasion Via Targeting the miR-137/AKT2 Axis

Li, Wei; Ge, Jinzhao; Xie, Jinju; Yang, Jinlong; Chen, Jine; He, Tao

doi:10.1089/cbr.2019.3297

Cited by 15 publications

(6 citation statements)

References 41 publications

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“…Shao et al showed that knockdown of TUG1 suppresses cell proliferation and migration through the KLF4/miR-153-1 axis [13]. Notably, TUG1 has also been demonstrated to promote cell migration, invasion, and proliferation in HCC through different pathways, such as the miR-29c-3p/COL1A1 axis [10], miR-137/AKT2 axis [22], and miR-144/JAK2/STAT3 axis [16]. However, the understanding of TUG1 in immune response regulation remains unknown.…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA TUG1 Inhibits Tumor Progression through Regulating Siglec-15-Related Anti-Immune Activity in Hepatocellular Carcinoma

Ren

Lyu

Guo

et al. 2022

Journal of Immunology Research

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Background. Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related death, and its biology remains poorly understood, especially in regards to the immunosuppression induced by immune checkpoints, such as Siglec-15. Most cancer treatments composed of immune checkpoint inhibitors and oncogene-targeted drugs display a better therapeutic effect in the clinic, including tumor progression inhibition and immunosuppression breaks. However, two or more drugs will result in a greater possibility of adverse effects. Thus, a double-function target is necessary for developing antitumor drugs, such as RNAi therapy. Methods. The expression of TUG1, Siglec-15, and miRNAs was evaluated by qPCR, and protein expression was analyzed by western blotting. The immune responses were evaluated by a Jurkat-reporter gene assay, a T cell-induced cytotoxicity assay, and IFN-γ/IL-2 release. The interactions among TUG1, Siglec-15, and miRNAs were verified by dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays. CCK-8 and Transwell assays were used to determine tumor cell proliferation, migration, and invasion. Results. In HCC patients and cells, increased TUG1 levels were observed, positively regulating Siglec-15 expression. TUG1-induced Siglec-15 upregulation resulted in the suppression of the immune response of HCC cells. hsa-miR-582-5p directly targeted TUG1 and Siglec-15 mRNA, and ihsa-miR-582-5p knockout prevented the regulation of Siglec-15 induced by THU1. Changes in hsa-miR-582-5p expression negatively regulated Siglec-15 levels and immunosuppression but had no influence on TUG1 levels. siRNA knockdown of TUG1 effectively led to tumor progression inhibition and immune response improvement in HCC cells both in vitro and in vivo. Conclusion. TUG1 increases the Siglec-15 level in HCC cells as a sponge to hsa-miR-582-5p, resulting in enhanced immunosuppression. TUG1 knockdown induced by siRNA not only reduces immunosuppression but also suppresses tumor progression both in vitro and in vivo. These novel findings may provide a potential and appropriate target for RNAi therapy to develop drugs with dual antitumor activity.

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Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA TUG1 Inhibits Tumor Progression through Regulating Siglec-15-Related Anti-Immune Activity in Hepatocellular Carcinoma

Ren

Lyu

Guo

et al. 2022

Journal of Immunology Research

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“…The same lncRNA can inhibit or promote tumor development in different cancer types. For example, TUG1 is a tumor suppressor in NSCLC and an oncogenic factor in hepatocellular carcinoma (W. Li et al, 2020; P. C. Lin et al, 2016). In osteosarcoma, a lncRNA may have contrary roles in different stage (Ulaner et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

LncRNA FGD5‐AS1 potentiates autophagy‐associated doxorubicin resistance by regulating the miR‐154‐5p/WNT5A axis in osteosarcoma

Fei

Yuan²,

Zhao

et al. 2022

Cell Biology International

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Osteosarcoma is prevalent in children and adolescent. The oncogenic function of long‐chain noncoding RNA (lncRNA) FGD5 antisense RNA 1 (FGD5‐AS1) has been reported. However, the function of FGD5‐AS1 in doxorubicin‐resistance in osteosarcoma remains to be illucidated. Quantitative real‐time PCR (qRT‐PCR) and western blot analysis (WB) were used to measure the expression of FGD5‐AS1, miR‐154‐5p, WNT5A and autophagy proteins. MTT assay was used to assess cell viability and transwell assay was performed to evaluate migration. A nude mouse xenograft model was developed to verify the function of FGD5‐AS1 in vivo. FGD5‐AS1 was upregulated in doxorubicin‐resistant (DXR) osteosarcoma cells. Knockdown of FGD5‐AS1 suppressed osteosarcoma cell proliferation, migration, and autophagy. FGD5‐AS1 upregulated WNT5A expression via sponging miR‐154‐5p. Furthermore, FGD5‐AS1 enhanced osteosarcoma cell chemotherapy resistance through upregulation of WNT5A by inhibiting miR‐154‐5p. Suppression of FGD5‐AS1 significantly suppressed tumor growth in nude mice. FGD5‐AS1 may promote chemoresistance through WNT5A‐induced autophagy by sponging miR‐154‐5p in osteosarcoma cells.

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“…In addition, lncRNAs also accomplish a predominant task in the proliferation, metastasis, and invasion of liver cancer. For example, lncRNA TUG1 is considerably expressed in hepatoma cells and augments the invasion and migration of hepatocellular carcinoma through targeting the miR-137/AKT2 axis [ 25 ]. The outcomes of the current survey illuminated that lncRNA ZNF674-AS1 was expressed at low level in liver cancer cells and tissues, and overexpression of lncRNA ZNF674-AS1 in liver cancer cells could substantially inhibit the proliferation, plate colony formation, migration, and invasion of liver cancer cells.…”

Section: Discussionmentioning

confidence: 99%

LncRNA ZNF674-AS1 Hinders Proliferation and Invasion of Hepatic Carcinoma Cells through the Glycolysis Pathway

Xie

Sun

et al. 2022

Journal of Oncology

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Purpose. Long noncoding RNAs (lncRNAs) play important roles in regulating various functions of cells at the levels of transcription and posttranscription. Extensive investigations have illustrated that lncRNAs are critical in the glucose metabolism of tumor cells, but their mechanisms of action need to be further explored. This study evaluates the role of lncRNA ZNF674-AS1 on the apoptosis and proliferation of human hepatic carcinoma cells in vitro through the glucose metabolism and its related mechanisms. Methods. Real-time quantitative PCR was employed for detecting the level of expressions for lncRNA ZNF674-AS1 in liver cancer tissues (25 cases), paracancerous tissues, and liver cancer cell lines. The lncRNA ZNF674-AS1 high expression cell strain was constructed by the lentiviral overexpression vector. CCK-8, plate colony formation, transwell assay, lactate production, glucose consumption, and ATP levels were used to detect the change of cell proliferation, colony formation, migration, and invasion, as well as glycolytic capability. Western blot was carried out to detect the expression of HK2, PFKL, PKM2, GLUT1, and PKM1, which are the key proteins of glycolysis in cells. Result. The lncRNA ZNF674-AS1 was undesirably expressed in liver cancer cell lines and tissues. Cell function assessments showed that compared with the blank control group (vector), overexpression of lncRNA ZNF674-AS1 could substantially hinder the proliferation, colony formation, migration, and invasion capability of liver cancer cells. Furthermore, overexpression of lncRNA ZNF674-AS1 could inhibit cell glycolysis (inhibit glucose consumption and reduce intracellular lactate and ATP levels) by inhibiting the expression of key proteins (such as PFKL, HK2, PKM2, and GLUT1) in the process of glycolysis. Conclusion. As a tumor repressor gene, lncRNA ZNF674-AS1 inhibits the expression of key proteins in glycolysis to inhibit glycolysis level, thereby inhibiting cell migration and proliferation. Therefore, lncRNA ZNF674-AS1 could be a potent therapeutic target or a novel diagnostic molecule for patients suffering from liver cancer.

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LncRNA TUG1 Promotes Hepatocellular Carcinoma Migration and Invasion Via Targeting the miR-137/AKT2 Axis

Cited by 15 publications

References 41 publications

Long Noncoding RNA TUG1 Inhibits Tumor Progression through Regulating Siglec-15-Related Anti-Immune Activity in Hepatocellular Carcinoma

Long Noncoding RNA TUG1 Inhibits Tumor Progression through Regulating Siglec-15-Related Anti-Immune Activity in Hepatocellular Carcinoma

LncRNA FGD5‐AS1 potentiates autophagy‐associated doxorubicin resistance by regulating the miR‐154‐5p/WNT5A axis in osteosarcoma

LncRNA ZNF674-AS1 Hinders Proliferation and Invasion of Hepatic Carcinoma Cells through the Glycolysis Pathway

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