Integration analysis for novel lncRNA markers predicting tumor recurrence in human colon adenocarcinoma

Chen, Fangyao; Li, Zhe; Deng, Chao; Yan, Hong

doi:10.1186/s12967-019-2049-2

Cited by 20 publications

(19 citation statements)

References 60 publications

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“…As STK4-AS1 was found to be a cancer "booster" in breast cancer [32], lung cancer [27], and colon cancer [26], we hypothesized that it also promoted the progression of osteosarcoma by p53/p21 pathway. MTT assay with transfected cells revealed that the expression of STK4-AS1 level was associated with cell viability, which was consistent with our hypothesis.…”

Section: Discussionmentioning

confidence: 99%

“…Osteosarcoma derives from primitive bone-forming mesenchymal cells [24] and it is also suggested to be regulated by lncRNAs [25]. An increasing number of lncRNAs were identi ed as the prognostic biomarkers or potential therapeutic targets of cancer by bioinformatics study [26,27] and the role of many of them in osteosarcoma has been validated in vivo or in vitro [28][29][30][31]. As the number of lncRNAs is large and the regulation network of lncRNAs is complex, more works are required in this eld.…”

Section: Introductionmentioning

confidence: 99%

“…A lncRNA, STK4-AS1, has previously been identi ed as a cancer biomarker associated with the progression of breast cancer [32], lung cancer [27], and colon cancer [26]. STK4-AS1 orientates from the minus strand and is located at 20q13.12 in the human genome with a size of 2,665 bases [33].…”

Section: Introductionmentioning

confidence: 99%

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LncRNA STK4 antisense RNA 1(STK4-AS1) affects the osteosarcoma cell cycle by regulating p53 protein

Yao

Hou

Liu

et al. 2021

Preprint

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Background: LncRNA STK4-AS1 has been identified as a potential biomarker associated with multiple cancers. We proposed that STK4-AS1 plays a role in the proliferation of osteosarcoma by regulating its cell cycle. Methods: We compared the expression of STK4-AS1 in osteosarcoma vs normal samples both in clinical tissues and cell lines. We overexpressed and knockdown STK4-AS1 in p53 expressing osteosarcoma cells U2OS and p53 muted expressing osteosarcoma cells MG63 and analyzed cell viability and cell cycle. We overexpressed p53 in STK4-AS1 knockdown cells to explore the association of STK4-AS1 and p53 in the cell cycle. Results: The STK4-AS1 expression was higher in osteosarcoma tissue than adjacent normal bone tissues and was higher in osteosarcoma cell lines (U2OS, MG63, and SAOS-2) than in osteoblast cell lines (hFOB and HOB). Knockdown of STK4-AS1 in U2OS decreased the cell viability, increased cells in the G0/G1 phase, decreased cells in the S and G2/M phase, decreased expression of cyclin A and B, increased p53 and p21, and had no effect on cyclin D and cyclin E, while overexpression did the opposes. MG63 cell viability was not affected by altered STK4-AS1 levels. P53 overexpression in STK4-AS1 knockdown cells recovered cell viability, p21, cyclin A, and cyclin B expression. Conclusion: LncRNA STK4-AS1 affected p53 expressing osteosarcoma cells U2OS cell viability through regulating cell cycle, which is mediated by p53/p21 pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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LncRNA STK4 antisense RNA 1(STK4-AS1) affects the osteosarcoma cell cycle by regulating p53 protein

Yao

Hou

Liu

et al. 2021

Preprint

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“…It is known that long non-coding RNAs (lncRNAs) are RNA molecules with more than 200 nucleotides [ 3 , 4 ]. Generally, lncRNAs modulate the expression level of targeted genes at the post-transcriptional period [ 5 ]. More and more lncRNAs have been found to involve in many aspects of cellular homeostasis, such as angiogenesis, metastasis, cell proliferation, immunity adjustment, genomic stability, and so on [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

LncRNA ACTA2-AS1 suppress colon adenocarcinoma progression by sponging miR-4428 upregulation BCL2L11

et al. 2021

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Background Long non-coding RNA is considered to be essential to modulate the development and progression of human malignant cancers. And long non-coding RNA can act as crucial modulators by sponging the corresponding microRNA in tumorigenesis. We aimed to elucidate the function of ACTA2-AS1 and its molecular mechanism in colon adenocarcinoma. Materials and methods The expression of ACTA2-AS1, miR-4428 and BCL2L11 in colon adenocarcinoma tissues were detected via qRT-PCR. SW480 and HT29 cells were transfected with shRNA ACTA2-AS1, OE ACTA2-AS1, miRNA mimics of miR-4428, miR-4428 inhibitor, si-BCL2L11 and over-expression of si-BCL2L11. Cell proliferation, colony formation and apoptosis were respectively assessed using CCK-8 assay, colony assay and flow cytometry. Luciferase reporter assay was performed to verify the targets of ACTA2-AS1 and miR-4428. Tumor subcutaneous xenograft mode was constructed to explore tumor growth in vivo. Results ACTA2-AS1 was obviously downregulated in human colon adenocarcinoma tissues and colon adenocarcinoma cell lines. Silence or over-expression of ACTA2-AS1 promoted or inhibited cell proliferation and colony formation abilities, and regulated apoptosis. The silence of ACTA2-AS1 resulted in the decrease of Bax and increase of Bal2, while restored in OE ACTA2-AS1 group when compared with the control transfected cells. In addition, luciferase reporter assay revealed that ACTA2-AS1 interacted with miR-4428 and suppressed its expression. miR-4428 could bind to 3ʹ untranslated region of BCL2L11 and modulated the expression of BCL2L11 negatively. Knockdown of ACTA2-AS1 and over-expression of BCL2L11 reversed the biological function that ACTA2-AS1 mediated by knockdown ACTA2-AS1 alone. Conclusion Our data demonstrated that ACTA2-AS1 could suppress colon adenocarcinoma progression via sponging miR-4428 to regulate BCL2L11 expression.

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“…However, there are few studies about ceRNAs based prediction models of COAD recurrence. In the study of Chen et al, they established ceRNA network for differentially expressed RNAs (DERs) between 15 non-recurrent and 98 recurrent COAD patients from The Cancer Genome Atlas (TCGA) database [16]. Meanwhile, Chen et al identified the prognostic lncRNA markers by using multivariate regression and established a nomogram for recurrence prediction based on the identified lncRNA biomarkers and clinical covariates [16].…”

Section: Introductionmentioning

confidence: 99%

Prognosis prediction model based on competing endogenous RNAs for recurrence of colon adenocarcinoma

et al. 2020

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Background Colon adenocarcinoma (COAD) patients who develop recurrence have poor prognosis. Our study aimed to establish effective prognosis prediction model based on competing endogenous RNAs (ceRNAs) for recurrence of COAD. Methods COAD expression profilings downloaded from The Cancer Genome Atlas (TCGA) were used as training dataset, and expression profilings of GSE29623 retrieved from Gene Expression Omnibus (GEO) were set as validation dataset. Differentially expressed RNAs (DERs) between non-recurrent and recurrent specimens in training dataset were screened, and optimum prognostic signature DERs were revealed to establish prognostic score (PS) model. Kaplan-Meier survival analysis was conducted for PS model, and GEO dataset was used for validation. Prognosis prediction efficiencies were evaluated by area under curve (AUC) and C-index. Meanwhile, ceRNA regulatory network was constructed by using signature mRNAs, lncRNAs and miRNAs. Results We identified 562 DERs including 42 lncRNAs, 36 miRNAs, and 484 mRNAs. PS prediction model, consisting of 17 optimum prognostic signature DERs, showed that high risk group had significantly poorer prognosis (5-year AUC = 0.951, C-index = 0.788), which also validated in GSE29623. Prognosis prediction model incorporating multi-RNAs with pathologic distant metastasis (M) and pathologic primary tumor (T) (5-year AUC = 0.969, C-index = 0.812) had better efficiency than clinical prognosis prediction model (5-year AUC = 0.712, C-index = 0.680). In the constructed ceRNA regulatory network, lncRNA NCBP2-AS1 could interact with hsa-miR-34c and hsa-miR-363, and lncRNA LINC00115 could interact with hsa-miR-363 and hsa-miR-4709. SIX4, GRAP, NKAIN4, MMAA, and ERVMER34–1 are regulated by hsa-miR-4709. Conclusion Prognosis prediction model incorporating multi-RNAs with pathologic M and pathologic T may have great value in COAD prognosis prediction.

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Integration analysis for novel lncRNA markers predicting tumor recurrence in human colon adenocarcinoma

Cited by 20 publications

References 60 publications

LncRNA STK4 antisense RNA 1(STK4-AS1) affects the osteosarcoma cell cycle by regulating p53 protein

LncRNA STK4 antisense RNA 1(STK4-AS1) affects the osteosarcoma cell cycle by regulating p53 protein

LncRNA ACTA2-AS1 suppress colon adenocarcinoma progression by sponging miR-4428 upregulation BCL2L11

Prognosis prediction model based on competing endogenous RNAs for recurrence of colon adenocarcinoma

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