WGCNA Co-Expression Network Analysis Reveals ILF3-AS1 Functions as a CeRNA to Regulate PTBP1 Expression by Sponging miR-29a in Gastric Cancer

Ren, Zhenhu; Shang, Gao-Pan; Wu, Kun; Hu, Chuanyu; Ji, Tong

doi:10.3389/fgene.2020.00039

Cited by 28 publications

(24 citation statements)

References 28 publications

(27 reference statements)

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“…17 Knockdown of ILF3-AS1 suppresses gastric cancer cell proliferation and metastasis. 18 However, the specific biological functions of ILF3-AS1 in breast cancer have not been investigated.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: ILF3-AS1 promotes cell proliferation and inhibits cell apoptosis of breast cancer by binding with miR-4429 to upregulate RAB14

et al. 2021

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As one of the leading causes of cancer-related deaths among women, breast cancer accounts for a 30% increase of incidence worldwide since 1970s. Recently, increasing studies have revealed that the long non-coding RNA ILF3-AS1 is involved in the progression of various cancers. Nevertheless, the role of ILF3-AS1 in breast cancer remains largely unknown. In the present study, we found that ILF3-AS1 was highly expressed in breast cancer tissues and cells. ILF3-AS1 silencing inhibited breast cancer cell proliferation, migration and invasion, and promoted cell apoptosis. ILF3-AS1 bound with miR-4429 in breast cancer cells. Moreover, RAB14 was a downstream target of miR-4429, and miR-4429 expression was negatively correlated with RAB14 or ILF3-AS1 expression in breast cancer tissues. The result of rescue experiments demonstrated that overexpression of RAB14 can reverse the inhibitory effect of ILF3-AS1 knockdown on breast cancer cell proliferation, migration and invasion. Overall, ILF3-AS1 promotes the malignant phenotypes of breast cancer cells by interacting with miR-4429 to regulate RAB14, which might offer a new insight into the underlying mechanism of breast cancer.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: ILF3-AS1 promotes cell proliferation and inhibits cell apoptosis of breast cancer by binding with miR-4429 to upregulate RAB14

et al. 2021

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“… 15 In gastric cancer, ILF3-AS1 promoted gastric cancer progression through the miR-29a/PTBP1 pathway. 16 In osteosarcoma, ILF3-AS1 regulated SOX5 expression through miR-212. 17 But the exact mechanism of action in colon cancer is not clear.…”

Section: Discussionmentioning

confidence: 99%

LncRNA ILF3-AS1 Promotes the Progression of Colon Adenocarcinoma Cells Through the miR-619-5p/CAMK1D Axis

Liu¹,

Li²

2021

OTT

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Introduction: Colon adenocarcinoma (COAD) is the third most common tumor of the digestive tract. Recent studies reported that lncRNA's abnormal expression might play a vital role in the occurrence and development of COAD. Methods: In the present study, we investigated the expression of ILF3-AS1 in COAD cell lines, human normal colon epithelial cell line, patient tumor tissues and adjacent normal tissues by real-time quantitative PCR (RT-qPCR). Small interfering RNAs (siRNAs) were transfected into COAD cells to inhibit the expression of ILF3-AS1. The effects of ILF3-AS1 on cell proliferation, migration, invasion and apoptosis were measured by CCK-8 assay, transwell migration and invasion assay, and flow cytometry apoptosis assay, respectively. The direct binding of ILF3-AS1 and miR-619-5p/CAMK1D was validated by the luciferase reporter assay. The expression of CAMK1D and epithelial-mesenchymal transformation (EMT)-related proteins was detected by Western Blot analysis. Besides, in vivo experiments were conducted to demonstrate the oncogenic role of ILF3-AS1 in COAD. Results: The results showed that the expression of ILF3-AS1 was significantly higher in COAD tissue than in normal adjacent samples, and this conclusion was confirmed in the available public datasets. After ILF3-AS1 knockdown, the proliferation of COAD cell lines SW480 and HT29 was significantly inhibited. At the same time, the apoptosis was increased, and the invasion and migration abilities were decreased. After further exploring the mechanisms, we found that ILF3-AS1 serves as a competitive endogenous RNA of mir-619-5p. It can bind to mir-619-5p and reduce its expression, thus regulating the target gene CAMK1D. In addition, we found that high expression of ILF3-AS1 was significantly associated with tumor grade, tumor size, and distant metastasis in COAD samples. In vivo experiments confirmed that ILF3-AS1 promotes tumor growth in COAD models. Conclusion: The present study demonstrated that ILF3-AS1 plays an oncogenic role in COAD through regulating the miR-619-5p/CAMK1D axis, and inhibition of ILF3-AS1 may pave the way for COAD treatment.

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“…Recently, increasing studies demonstrate that lncRNAs can directly interacts with miRNAs to modulate their downstream target expressions in GC progression [26,27]. For instance, lncRNA MALAT1 directly interacts with miR-22-3p to modulate zinc finger protein 91 (ZFP91) expression in GC cells [26], and lncRNA ILF3-AS1 functions as a ceRNA via sponging miR-29a to elevate PTBP3 expression in GC cells [27]. Interestingly, lncRNA LINC00504 acts as a molecular sponge for miR-1244 to modulate aerobic glycolysis in ovarian cancer [28].…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC01391 restrained gastric cancer aerobic glycolysis and tumorigenesis via targeting miR-12116/CMTM2 axis

Qian

Chen

et al. 2020

J. Cancer

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Increasing studies indicate that long noncoding RNA (lncRNA) plays a critical role in aerobic glycolysis of various tumors. However, the contribution of lncRNA in gastric cancer (GC) cell glycolysis is still poorly understood. The objective of this research was to investigate the functional role and mechanism of lncRNA long intergenic non-protein coding RNA 1391 (LINC01391) in the aerobic glycolysis and tumorigenesis of GC. Here, we report that LINC01391 was low expressed in GC tissues and cell lines. LINC01391 overexpression hampered GC cell proliferation, migration, invasion and aerobic glycolysis, while LINC01391 knockdown demonstrated the opposite effects. LINC01391 overexpression delayed the tumor growth in vivo. Furthermore, LINC01391 interacted with miR-12116, and miR-12116 interacted with CMTM2 in GC cells. And miR-12116 and CMTM2 participated in the inhibitory effects of LINC01391 on cell migration, invasion and aerobic glycolysis in GC cells. LINC01391 restrained aerobic glycolysis and tumorigenesis of GC via targeting miR-12116/CMTM2 axis, which provides new insights into mechanism of GC progression.

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WGCNA Co-Expression Network Analysis Reveals ILF3-AS1 Functions as a CeRNA to Regulate PTBP1 Expression by Sponging miR-29a in Gastric Cancer

Cited by 28 publications

References 28 publications

RETRACTED: ILF3-AS1 promotes cell proliferation and inhibits cell apoptosis of breast cancer by binding with miR-4429 to upregulate RAB14

RETRACTED: ILF3-AS1 promotes cell proliferation and inhibits cell apoptosis of breast cancer by binding with miR-4429 to upregulate RAB14

LncRNA ILF3-AS1 Promotes the Progression of Colon Adenocarcinoma Cells Through the miR-619-5p/CAMK1D Axis

Long noncoding RNA LINC01391 restrained gastric cancer aerobic glycolysis and tumorigenesis via targeting miR-12116/CMTM2 axis

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