LncRNA CCAT2 promotes the proliferation and invasion of renal cell cancer by sponging miR-320a

Wu, Guoyu; Ke, Jianlong; Wang, Jinyang; Zhu, Xi; Xiong, Shuping

doi:10.23736/s0031-0808.19.03778-9

Cited by 4 publications

(3 citation statements)

References 4 publications

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“…Also, Cheng C et al have found that miR-26a-5p is knocked down in RCC, and it curbs RCC cell proliferation and invasion and intensifies cell death by targeting E2F7 (Cheng et al, 2020). miR-320a has been found sponged by lncRNA CCAT2 (Wu et al, 2020), but its downstream mechanism in RCC progression needs further investigation.…”

Section: Introductionmentioning

confidence: 99%

HIF-1α Induces HECTD2 Up-Regulation and Aggravates the Malignant Progression of Renal Cell Cancer via Repressing miR-320a

Shen

Yao

et al. 2021

Front. Cell Dev. Biol.

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Renal cell carcinoma (RCC) is a frequent malignancy of the urinary system. It has been found that hypoxia mediates the malignant evolvement of RCC. Here, we probe the impact and potential mechanism of HECT domain E3 ubiquitin-protein ligase 2 (HECTD2) and HIF-1α on regulating RCC evolvement. RCC tissues and adjacent normal tissues were collected, and the association between the expression profiles of HECTD2 and HIF-1α and the clinicopathological features was analyzed. Additionally, we constructed HECTD2/HIF-1α overexpression and knockdown models in RCC cell lines to ascertain the impacts of HECTD2 and HIF-1α on RCC cell proliferation, apoptosis, migration, and growth in vivo. We applied bioinformatics to predict the upstream miRNA targets of HECTD2. Meanwhile, RNA immunoprecipitation (RIP), and the dual-luciferase reporter assays were employed to clarify the targeting association between HECTD2 and miR-320a. The effect of miR-320a on HECTD2-mediated RCC progression was investigated. The results suggested that both HIF-1α and HECTD2 were up-regulated in RCC (compared with adjacent non-tumor tissues), and they had positive relationship. Moreover, higher level of HECTD2 and HIF-1α is associated with poorer overall survival of RCC patients. HECTD2 overexpression heightened RCC cell proliferation and migration, and weakened cell apoptosis. On the other hand, the malignant phenotypes of RCC cells were signally impeded by HECTD2 or HIF-1α knockdown. Moreover, miR-320a targeted the 3′-untranslated region of HECTD2 and suppressed HECTD2 expression. The rescue experiments showed that miR-320a restrained HECTD2-mediated malignant progression in RCC, while up-regulation of HIF-1α hampered miR-320a expression. Collectively, HIF-1α mediated HECTD2 up-regulation and aggravated RCC progression by attenuating miR-320a.

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Section: Introductionmentioning

confidence: 99%

HIF-1α Induces HECTD2 Up-Regulation and Aggravates the Malignant Progression of Renal Cell Cancer via Repressing miR-320a

Shen

Yao

et al. 2021

Front. Cell Dev. Biol.

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“…He et al [ 74 ] used a mouse xenograft model and showed that knocking out the expression of CCAT2 can inhibit the growth of xenografts. In 2019, Wu et al [ 75 ] pointed out that knocking out CCAT2 could inhibit cell proliferation, colony formation, and invasion. Moreover, CCAT2 can promote the proliferative and invasive abilities of renal cell carcinoma cells by interacting with miR-320a.…”

Section: Ccat2 In Human Cancersmentioning

confidence: 99%

“…Moreover, the integration of CCAT2, b2-MG, HGB, and IgA was found to considerably improve the AUC value and sensitivity of MM diagnosis. In cervical cancer, Osteosarcoma miR-200b/VEGF; miR-143 [56,57] Endometrial cancer miR-216b/Bcl-2 [28] Breast cancer miR-205 [15] Overian cancer miR-424/Notch2 [65] Hepatoocellular carcinoma miR-34a/FOXM1; miR-145/MDM2 [27,50] PC miR-217 [74] Renal cell carcinoma miR-145/p70s6k1 [47] EC miR-320a [75] CRC Pre-miR-145; miR-20a; miR-21; miR-17-5p; miR-145 [7,41] EMT PC N-cadherin/Vimentin/E-cadherin [73] GC E-cadherin/Vimentin/N-cadherin/EZH2 [24] Hepatoocellular carcinoma Vimentin/E-cadherin/SNAIL2 [49] Glioma E-cadherin/Vimentin/N-cadherin/ Twist/b-catenin/Snail [71] Ovarian cancer E-cadherin/N-cadherin/Snail/Twist [67] CCA E-cadherin/Vimentin [53] Interaction with protein molecules Breast cancer EZH2/p15 [16] CRC Myc/BOP1/AURKB [6] Pituitary tumors PTTG1/SOX2/DLK1/MMP2/MMP13 [79] Signal pathway Wnt/b-catenin signal pathway Lung cancer b-catenin [22] OSCC b-catenin/Cyclin D1/Myc [77] Renal cell carcinoma b-catenin/c-Myc/Cyclin D1 [74] Ovarian cancer b-catenin/c-Myc [66,67] EC b-catenin/Cyclin D1/c-Myc [46] PC b-catenin/Cyclin D1/c-Myc [74] TC b-catenin/c-Myc/Cyclin D1 [3] Breast cancer b-catenin/Cyclin D1/c-Myc [69] Glioma b-catenin/c-Myc/CyclinD1 [20] Colon cancer b-catenin [7] PI3K/Akt signal pathway Endometrial cancer PI3K/Akt/mTOR [28] GC PI3K/mTOR [12,13] Osteosarcoma PI3K/Akt [56] Gliomas PI3K/Akt…”

Section: Role Of Ccat2 As a Biomarker For Cancer Diagnosismentioning

confidence: 99%

Long non-coding RNA colon cancer-associated transcript 2: role and function in human cancers

Wang

Zhang

et al. 2023

Chinese Medical Journal

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Long non-coding RNAs (lncRNAs) are a family of non-protein-coding RNAs that span a length of over 200 nucleotides. Research reports have illustrated that lncRNAs are involved in various cellular processes and that their abnormal expression leads to the occurrence and development of various tumors. Colon cancer-associated transcript 2 (CCAT2) was first reported as an oncogene in colon cancer. LncRNA CCAT2 is abnormally expressed in hepatocellular carcinoma, cholangiocarcinoma, lung cancer, breast cancer, ovarian cancer, glioma, and other tumors. In tumor tissues, abnormally overexpressed CCAT2 can affect cell proliferation, migration, epithelial-mesenchymal transition, apoptosis, and other biological behaviors through endogenous RNAs mechanisms, various signaling pathways, transcriptional regulation, and other complex mechanisms. Additionally, the overexpression of CCAT2 is also closely related to the tumor size, tumor node metastasis (TNM) stage, survival time, and other prognostic factors, suggesting that it is a potential prognostic indicator. This article reviews the biological functions of CCAT2 and its mechanisms of action in tumors from previous studies. In this review, we attempt to provide a molecular basis for future clinical applications of lncRNA CCAT2.

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LncRNA CCAT2 promotes malignant progression of metastatic gastric cancer through regulating CD44 alternative splicing

et al. 2023

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LncRNA CCAT2 promotes the proliferation and invasion of renal cell cancer by sponging miR-320a

Cited by 4 publications

References 4 publications

HIF-1α Induces HECTD2 Up-Regulation and Aggravates the Malignant Progression of Renal Cell Cancer via Repressing miR-320a

HIF-1α Induces HECTD2 Up-Regulation and Aggravates the Malignant Progression of Renal Cell Cancer via Repressing miR-320a

Long non-coding RNA colon cancer-associated transcript 2: role and function in human cancers

LncRNA CCAT2 promotes malignant progression of metastatic gastric cancer through regulating CD44 alternative splicing

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