Upregulated lncRNA DLX6-AS1 underpins hepatocellular carcinoma progression via the miR-513c/Cul4A/ANXA10 axis

Liu, Xiaoming; Peng, Dandan; Cao, Yixin; Zhu, Yuanzhe; Yin, Jianjun; Zhang, Guangxing; Peng, Xiao-Dong; Yang, Meng

doi:10.1038/s41417-020-00233-0

Cited by 23 publications

(16 citation statements)

References 28 publications

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“…lncRNAs play an important role in a variety of physiological and pathological processes such as cell proliferation and apoptosis, cell proliferation and senescence, immune activation and inactivation ( 7 , 8 ). Multiple lncRNAs have been confirmed by previous studies to play a vital role in HCC, such as TMPO-AS1 ( 9 ), MYLK-AS1 ( 10 ) and DLX6-AS1 ( 11 ). However, there are relatively few reports on the role of lncRNA MT1JP in HCC, and its ability to predict the prognosis of this disease is still limited.…”

Section: Introductionmentioning

confidence: 54%

lncRNA MT1JP‑overexpression abolishes the silencing of PTEN by miR‑32 in hepatocellular carcinoma

Zhang

Chen

et al. 2021

Oncol Lett

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Previous studies have shown that long non-coding RNA (lncRNA) MT1JP plays a role as a tumor suppressor in several types of cancer. The present study aimed to explore the role of MT1JP in hepatocellular carcinoma (HCC). Paired HCC and non-tumor tissues from 64 patients with HCC were subjected to RNA isolation and reverse transcription-quantitative PCR (RT-qPCR) to analyze the differential expression of MT1JP, microRNA (miR)-32 and phosphatase and tensin homolog (PTEN) in HCC. Cell transfections, followed by RT-qPCR and western blotting, were carried out to investigate the interactions among MT1JP, miR-32 and PTEN. The role of MT1JP, miR-32 and PTEN in regulating HCC cell proliferation was assessed using a Cell Counting Kit-8 assay. It was found that MT1JP was downregulated in HCC cancer tissues compared with that in non-cancer tissues. Survival analysis showed that patients with low MT1JP expression levels exhibited a significantly higher 5-year overall survival rate compared with patients with high MT1JP levels. The expression of MT1JP in HCC tissues was positively associated with PTEN and negatively associated with miR-32. Overexpression of MT1JP increased the expression levels of PTEN and decreased the expression levels of miR-32. Overexpression of miR-32 did not affect the expression of MT1JP but decreased the expression levels of PTEN and attenuated the effect of overexpression of MT1JP on the expression of PTEN. Overexpression of MT1JP and PTEN decreased the proliferation of HCC cells. Overexpression of miR-32 played an opposite role and attenuated the effects of overexpression of MT1JP. Therefore, MT1JP may upregulate PTEN by downregulating miR-32 to regulate HCC cell proliferation.

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Section: Introductionmentioning

confidence: 54%

lncRNA MT1JP‑overexpression abolishes the silencing of PTEN by miR‑32 in hepatocellular carcinoma

Zhang

Chen

et al. 2021

Oncol Lett

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“…cn/, Figure 1E). miR-513c-5p has been reported to be a significant cancer suppressor in various cancers 13,[22][23][24][25][26] other than THCA, suggesting its potential suppressive role in THCA.…”

Section: Resultsmentioning

confidence: 99%

TNRC6C-AS1 Promotes Thyroid Cancer Progression by Upregulating LPAR5 via miR-513c-5p

Tong

Wang

et al. 2021

CMAR

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Background Considering the combined role of long non-coding RNA (lncRNAs)-microRNA (miRNA)-mRNA in tumorigenesis, the purpose of this study was to investigate how TNRC6C-AS1 regulates the expression of lysophosphatidic acid receptor 5 (LPAR5) by modulating miR-513c-5p, thus influencing the progression of thyroid cancer (THCA). Methods qRT-PCR and Western blotting were performed to detect the expression levels of TNRC6C-AS1, miR-513c-5p, and LPAR5 in THCA tissues and cell lines. The viability, proliferation, migration, and invasion were assessed using CCK-8, BrdU, wound healing, and transwell migration assays, respectively. Dual-luciferase reporter assay, RIP assay, and RNA pull-down assay were used to evaluate the relationship between TNRC6C-AS1, miR-513c-5p, and LPAR5. Results TNRC6C-AS1 was highly expressed in THCA tissues, and knockout of TNRC6C-AS1 reduced the viability, proliferation, migration, and invasion of THCA cells. TNRC6C-AS1 competitively adsorbed miR-513c-5p. In addition, the biological function of TNRC6C-AS1 was blocked by knocking down the thyroid cell line TNRC6C-AS1 with miR-513c-5p inhibitor transfection. LPAR5 is the target gene for miR-513c-5p, which has the ability to eliminate the influence of miR-513c-5p on THCA cells. Conclusion The TNRC6C-AS1/miR-513c-5p/LPAR5 axis is a novel signaling pathway that modulates THCA progression and may be a potential target for cancer therapy.

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“…MiR-513c-5p was shown to act as a tumor regulator in various cancers, such as glioblastoma, hepatocellular carcinoma, and neuroblastoma, by modulating cell viability, cell cycle, invasion, migration, and apoptosis [31][32][33]. Moreover, miR-514b-5p expression was shown to be significantly elevated in colorectal cancer, which may play a role in accelerating tumor metastasis [34].…”

Section: Discussionmentioning

confidence: 99%

Positive feedback between lncRNA FLVCR1-AS1 and KLF10 may inhibit pancreatic cancer progression via the PTEN/AKT pathway

Lin

Zhai

Zou

et al. 2021

J Exp Clin Cancer Res

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Background FLVCR1-AS1 is a key regulator of cancer progression. However, the biological functions and underlying molecular mechanisms of pancreatic cancer (PC) remain unknown. Methods FLVCR1-AS1 expression levels in 77 PC tissues and matched non-tumor tissues were analyzed by qRT-PCR. Moreover, the role of FLVCR1-AS1 in PC cell proliferation, cell cycle, and migration was verified via functional in vitro and in vivo experiments. Further, the potential competitive endogenous RNA (ceRNA) network between FLVCR1-AS1 and KLF10, as well as FLVCR1-AS1 transcription levels, were investigated. Results FLVCR1-AS1 expression was low in both PC tissues and PC cell lines, and FLVCR1-AS1 downregulation was associated with a worse prognosis in patients with PC. Functional experiments demonstrated that FLVCR1-AS1 overexpression significantly suppressed PC cell proliferation, cell cycle, and migration both in vitro and in vivo. Mechanistic investigations revealed that FLVCR1-AS1 acts as a ceRNA to sequester miR-513c-5p or miR-514b-5p from the sponging KLF10 mRNA, thereby relieving their suppressive effects on KLF10 expression. Additionally, FLVCR1-AS1 was shown to be a direct transcriptional target of KLF10. Conclusions Our research suggests that FLVCR1-AS1 plays a tumor-suppressive role in PC by inhibiting proliferation, cell cycle, and migration through a positive feedback loop with KLF10, thereby providing a novel therapeutic strategy for PC treatment.

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Upregulated lncRNA DLX6-AS1 underpins hepatocellular carcinoma progression via the miR-513c/Cul4A/ANXA10 axis

Cited by 23 publications

References 28 publications

lncRNA MT1JP‑overexpression abolishes the silencing of PTEN by miR‑32 in hepatocellular carcinoma

lncRNA MT1JP‑overexpression abolishes the silencing of PTEN by miR‑32 in hepatocellular carcinoma

TNRC6C-AS1 Promotes Thyroid Cancer Progression by Upregulating LPAR5 via miR-513c-5p

Positive feedback between lncRNA FLVCR1-AS1 and KLF10 may inhibit pancreatic cancer progression via the PTEN/AKT pathway

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