LncRNA TP73-AS1 accelerates tumor progression in gastric cancer through regulating miR-194-5p/SDAD1 axis

Ding, Zhi; Lan, Haitao; Rui, Xu; Zhou, Xiang; Pan, Yong

doi:10.1016/j.prp.2018.09.006

Cited by 33 publications

(23 citation statements)

References 30 publications

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“…Elevated expression of NNT-AS1 promoted GC cell proliferation, cell cycle progression, and invasion [25]. Another study also demonstrated that TP73-AS1 accelerates cell growth and metastasis in GC [26]. Interestingly, TPT1-AS1 was proved to promote ovarian cancer tumor growth and metastasis through the downstream PI3K/AKT signaling pathway [19].…”

Section: Discussionmentioning

confidence: 96%

Knockdown of TPT1-AS1 inhibits cell proliferation, cell cycle G1/S transition, and epithelial–mesenchymal transition in gastric cancer

Tang

Huang

Wang

et al. 2020

Bosn J of Basic Med Sci

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Long non-coding RNAs are considered to be critical regulators of tumor progression. Tumor protein translationally controlled 1 antisense RNA 1 (TPT1-AS1) was shown to have an oncogenic role in cervical and ovarian cancer. The clinical significance and biological function of TPT1-AS1 in gastric cancer (GC) are not clear. In this study, we analyzed the expression of TPT1-AS1 in GC tissues and cell lines and performed functional and mechanistic analysis of TPT1-AS1 effects on GC cell proliferation, migration, and invasion. TPT1-AS1 expression was determined in 76 pairs of GC tissues vs. matched adjacent normal tissues and in four GC cell lines (SGC-7901, AGS, BGC-823, and MGC-803) vs. GES-1 cell line by quantitative reverse transcription PCR. SGC-7901 and MGC-803 cells were transfected with small interfering RNA or scrambled negative control, and cell proliferation, colony formation, migration, invasion and cell cycle assays were performed. The expression of proteins involved in cell cycle progression and epithelial–mesenchymal transition was analyzed by Western blot. TPT1-AS1 expression was significantly higher in GC tissues and cell lines compared to controls. The overexpression of TPT1-AS1 was significantly correlated with TNM stage and lymph node metastasis, and it was associated with worse prognosis of GC patients according to the Kaplan–Meier survival analysis and Cox proportional hazard regression analysis. The knockdown of TPT1-AS1 significantly inhibited proliferation, cell cycle G1/S transition, migration, and invasion of SGC-7901 and MGC-803 cells. Moreover, TPT1-AS1 knockdown downregulated the expression of CDK4, cyclin D1, and vimentin and upregulated the expression of p21 and E-cadherin. Our findings suggest that TPT1-AS1 may be a promising therapeutic target in GC.

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Section: Discussionmentioning

confidence: 96%

Knockdown of TPT1-AS1 inhibits cell proliferation, cell cycle G1/S transition, and epithelial–mesenchymal transition in gastric cancer

Tang

Huang

Wang

et al. 2020

Bosn J of Basic Med Sci

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“…15 Previous studies reported that TP73-AS1 was closely associated with tumor progression and poor prognosis in esophageal squamous cell carcinoma, breast cancer, brain glioma, gastric cancer and hepatocellular carcinoma. [16][17][18][19][20][21][22][23] These reports demonstrated that lncRNA TP73-AS1 acted as one oncogene in the tumorigenesis of cancer. Unfortunately, the biological function and underlying mechanism of lncRNA TP73-AS1 in lung adenocarcinoma are rarely explored and more researches are needed to be clarified.…”

Section: Introductionmentioning

confidence: 99%

<p>Knockdown Of Long Non-Coding RNA TP73-AS1 Inhibited Cell Proliferation And Metastasis Through Wnt/β-Catenin Pathway In Lung Adenocarcinoma</p>

Peng¹,

Xu²,

Yang³

et al. 2019

OTT

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Background: Various evidences showed that abnormally expressed long non-coding RNAs (lncRNAs) play important roles in the tumorigenesis and progression of malignancies. However, the exact role and regulatory mechanism of lncRNA TP73-AS1 in the pathogenesis and progression of lung adenocarcinoma remain to be further elucidated. Purpose: The aim of this study was to investigate the functional role and underlying mechanism of lncRNA TP73-AS1 in lung adenocarcinoma progression. Methods: RT-PCR assay was employed to detect TP73-AS1 expression in lung adenocarcinoma tissues and cells. The function of TP73-AS1 in lung adenocarcinoma progression was estimated by MTT assay, EdU assay, flow cytometry, Western blot, wound-healing assay and transwell assay. Results: LncRNA TP73-AS1 expression was significantly increased in lung adenocarcinoma tissues and cell lines. Moreover, functional assays revealed that silencing of lncRNA TP73-AS1 could attenuate cell proliferation, migration, invasion and epithelial-mesenchymal transition of lung adenocarcinoma, while enhanced expression of lncRNA TP73-AS1 led to the opposite results. Additionally, lncRNA TP73-AS1 knockdown could facilitate cell apoptosis and overexpression of lncRNA TP73-AS1 inhibited cell apoptosis. In addition, we further determined that lncRNA TP73-AS1 regulated cell metastasis through inducing the activation of Wnt/β-catenin signaling pathway in lung adenocarcinoma. Conclusion: Our results indicated that lncRNA TP73-AS1 may play an oncogenic role in lung adenocarcinoma progression, which provided a promising therapy strategy for the treatment of lung adenocarcinoma.

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“…For example, lncRNA H19 promotes the development of non‐small cell lung cancer via sponging miRNA‐107 (Qian et al, 2018). LncRNA TP73‐AS1 aggravates gastric cancer cell growth and metastasis via targeting miR‐194‐5p/SDAD1 axis (Ding, et al, 2018). LncRNA ADAMTS9‐AS2 sponges miR‐182‐5p to modulate ovarian cancer progression via upregulation of FOXF2 (A. Wang, et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

LINC00667 promotes Wilms’ tumor metastasis and stemness by sponging miR‐200b/c/429 family to regulate IKK‐β

Liu

Chen

Huang

et al. 2020

Cell Biology International

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Wilms' tumor, also known as nephroblastoma, is a kind of pediatric renal cancer. Previous studies have indicated that microRNAs (miRNAs) regulate various cancers progression. However, whether miR-200 family regulated Wilms' tumor progression remains to be elucidated. In our study, miR-200b/c/429 expression was downregulated in Wilms' tumor tissue samples from 25 patients. And data from three independent analyses of quantitative real-time polymerase chain reaction revealed that the expression of miR-200b/c/429 was downregulated in Wilms' tumor cell lines. Functionally, Cell counting kit-8 assay revealed that cell viability was reduced by overexpressing miR-200b/c/429. Transwell assay manifested that cell migration and invasion was hindered by miR-200b/c/429 overexpression. Sphere-forming and western blot assays demonstrated that miR-200b/c/429 overexpression suppressed the sphere formation ability. Mechanically, nuclear factor-κB (NF-κB) pathway was confirmed to be associated with Wilms' tumor progression; miR-200b/c/429 overexpression inactivated NF-κB pathway as miR-200b/c/429 was identified to target IκB kinase β (IKK-β), an NF-κB pathway-related gene. Moreover, miR-200b/c/429 was sponged by LINC00667 in Wilms' tumor cells. LINC00667 competitively bound with miR-200b/c/429 to regulate IKK-β expression and then activated NF-κB pathway in Wilms' tumor. Subsequently, rescue assays illustrated that silencing of IKK-β could reverse the effect of miR-200b/c/429 inhibition on the progression of sh-LINC00667-transfected Wilms' tumor cells. In summary, LINC00667 promoted Wilms' tumor progression by sponging miR-200b/c/429 family to regulate IKK-β.

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LncRNA TP73-AS1 accelerates tumor progression in gastric cancer through regulating miR-194-5p/SDAD1 axis

Cited by 33 publications

References 30 publications

Knockdown of TPT1-AS1 inhibits cell proliferation, cell cycle G1/S transition, and epithelial–mesenchymal transition in gastric cancer

Knockdown of TPT1-AS1 inhibits cell proliferation, cell cycle G1/S transition, and epithelial–mesenchymal transition in gastric cancer

<p>Knockdown Of Long Non-Coding RNA TP73-AS1 Inhibited Cell Proliferation And Metastasis Through Wnt/β-Catenin Pathway In Lung Adenocarcinoma</p>

LINC00667 promotes Wilms’ tumor metastasis and stemness by sponging miR‐200b/c/429 family to regulate IKK‐β

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