LncRNA PLAC2 upregulates p53 to induce hepatocellular carcinoma cell apoptosis

Zheng, Yajuan; Lv, Pengxiang; Wang, Shaoping; Cai, Qing; Bao, Zhenmin; Han, Feng

doi:10.1016/j.gene.2019.143944

Cited by 16 publications

(19 citation statements)

References 26 publications

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“…9 The loss of functional p53 is a prerequisite for oncogenesis to promote growth and proliferation and is the most common anomaly in human cancers, including HCC. 10 Various stress signals stabilise and activate p53, which exerts a tumour-suppressive function. 9,11 Mutations in the p53 gene are found in 50% of human tumours, 12 highlighting the importance of p53 in tumour suppression.…”

Section: Introductionmentioning

confidence: 99%

“…11,13 p53 mutations are considered to be major drivers of various cancers, including HCC. 9,10 The TCGA database indicates that p53 is uniformly mutated in 28.49% HCC. However, it is unclear whether p53 mutation can promote hyperactivated mTOR-driven HCC, and how to treat the subset of patients with HCC with mTOR activation and p53 mutations is also unresolved.…”

Section: Introductionmentioning

confidence: 99%

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p53 haploinsufficiency and increased mTOR signalling define a subset of aggressive hepatocellular carcinoma

Luo

Fang

et al. 2021

Journal of Hepatology

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Liver tumorigenesis Lung metastasis p53 mut/+ Highlights Tsc1 deficiency facilitates p53 (haplo)insufficiency-mediated activation of the PTEN/Akt/mTOR axis to drive HCC tumorigenesis and metastasis. Inhibiting mTOR activation is a potential therapeutic strategy for p53 insufficiency and Tsc1 insufficiency-driven hepatocarcinogenesis. The oncogenic activity of the Akt/mTOR axis relies on Abcc4, which labels an aggressive subtype of human HCC.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

p53 haploinsufficiency and increased mTOR signalling define a subset of aggressive hepatocellular carcinoma

Luo

Fang

et al. 2021

Journal of Hepatology

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“…14 PLAC 2 upregulates p53 in hepatocellular carcinoma to induce cell apoptosis. 15 In contrast, PLAC 2 activates Wnt/β-catenin pathway to promote cell proliferation in oral squamous cell carcinoma. 16 Therefore, PLAC 2 may play different roles in different cancers.…”

Section: Discussionmentioning

confidence: 99%

<p>LncRNA PLAC 2 Is Downregulated in Osteosarcoma and Regulates Cancer Cell Proliferation Through miR-93</p>

Sun

Shi

et al. 2020

CMAR

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Introduction: PLAC 2 is a tumor-suppressive lncRNA in glioma, while its roles in other types of cancer remain unclear. This study was carried out to explore the potential involvement of PLAC 2 in osteosarcoma (OS). Methods: Expression levels of PLAC 2 in OS and paired non-tumor tissues from OS patients were determined by RT-qPCR. A follow-up study was performed to analyze the prognostic value of PLAC 2 for OS. Interactions between PLAC 2 and miR-93 were assessed by cell transfection, followed by RT-qPCR. Cell proliferation assay was performed to analyze cell proliferation. Results: Our results showed that PLAC 2 was downregulated in OS tissues, and the high expression levels of PLAC 2 were associated with favorable overall survival of OS patients. MiR-93 was upregulated in OS tissues and its expression was inversely correlated with the expression of PLAC 2. In OS cells, overexpression of PLAC 2 resulted in downregulated miR-93, while overexpression of miR-93 did not affect the expression of PLAC 2. Overexpression of PLAC 2 led to decreased proliferation rate of OS cells, while overexpression of miR-93 showed opposite roles and reduced the overexpressing effects of PLAC 2. Conclusion: PLAC 2 is downregulated in OS and regulates cancer cell proliferation through miR-93.

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“…In HCC, two distinct studies showed association between over-expression of this lncRNA and induction of apoptosis via regulation of P53 and enhancement of cell proliferation via modulation of the miR-214-5p/ROCK1 axis, respectively [ 16 , 17 ]. Consistent with the latter study, depletion of this lncRNA in other HCC cell liens decreased oncogenic behavior through modulation of miR‐218‐5p/DDX5/AKT signaling [ 18 ].…”

Section: Cell Line Studiesmentioning

confidence: 99%

“…However, other studies have demonstrated down-regulated of TINCR in glioma, retinoblastoma and prostate cancer [ 5 , 25 , 26 ]. Notably, data regarding expression profile of this lncRNA in a number of human cancers such as colon cancer, squamous cell carcinoma, non-small cell lung cancer and HCC are controversial [ 7 , 12 , [14] , [15] , [16] , 22 , 23 , 30 ]. Expression level of this lncRNA has been associated with clinical outcome in patients with gastric cancer [ 6 ], colorectal cancer [ 12 ], head and neck SCC [ 24 ], non-small cell lung cancer [ 14 ] and some other cancers.…”

Section: Human Studiesmentioning

confidence: 99%

TINCR: An lncRNA with dual functions in the carcinogenesis process

Ghafouri‐Fard

Dashti

Taheri

et al. 2020

Non-coding RNA Research

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Long non-coding RNAs (lncRNAs) have prominent roles in the pathogenesis of human cancers. Several studies have shown oncogenic or tumor suppressor roles of lncRNAs in different human tissues. Thus, these transcripts have been regarded as putative targets in treatment of cancer. The lncRNA terminal differentiation-induced non-coding RNA (TINCR) has an especial position in this regard, as it exerts different opposite roles in the pathogenesis of different human cancers. While it is up-regulated in gastric, esophageal, bladder and breast cancer; it is down-regulated in glioma, retinoblastoma and prostate cancer. Notably, data regarding expression profile of this lncRNA in a number of human cancers such as colon cancer, squamous cell carcinoma, non-small cell lung cancer (NSCLC) and hepatocellular carcinoma (HCC) are controversial. Expression level of this lncRNA has been associated with clinical outcome in patients with gastric cancer, colorectal cancer, NSCLC and head and neck squamous cell carcinoma. Moreover, Kaplan-Meier analyses have shown correlation between expression levels of TINCR and patients survival in patients with lung cancer and HCC. A number of cellular pathways such as Wnt/β-catenin, ERK1/2‐SP3 and MAPK signaling pathways have been identified as targets of this lncRNA in different cancers. Moreover, the rs8113645, rs2288947 and rs8105637 within this lncRNA have been associated with risk of gastric and colorectal cancer. In conclusion, although the role of TINCR in the carcinogenesis is essential, based on the conflicting data regarding the direction of effect of this lncRNA, therapeutic targeting of this lncRNA is a complicated issue which should be considered in a tissue-specific or even individualized manner.

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LncRNA PLAC2 upregulates p53 to induce hepatocellular carcinoma cell apoptosis

Cited by 16 publications

References 26 publications

p53 haploinsufficiency and increased mTOR signalling define a subset of aggressive hepatocellular carcinoma

p53 haploinsufficiency and increased mTOR signalling define a subset of aggressive hepatocellular carcinoma

<p>LncRNA PLAC 2 Is Downregulated in Osteosarcoma and Regulates Cancer Cell Proliferation Through miR-93</p>

TINCR: An lncRNA with dual functions in the carcinogenesis process

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