lncARSR sponges miR‐34a‐5p to promote colorectal cancer invasion and metastasis via hexokinase‐1‐mediated glycolysis

Li, Shuai; Zhu, Kongxi; Liu, Lan; Gu, Jing; Niu, Huanmin; Guo, Jianqiang

doi:10.1111/cas.14617

Cited by 36 publications

(29 citation statements)

References 21 publications

(26 reference statements)

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“…For example, miR-122-5p can promote proliferation and invasion of renal cancer cells by targeting PKM2 (a glycolytic limiting enzyme) [ 65 ]. LncARSR-miR-34a-5p-HK1 axis (HK is another glycolytic limiting enzyme) facilitates the progression of rectal cancer by promoting glycolysis metabolism [ 66 ]. In summary, our discoveries provide new insights into the roles of glycolytic genes in RCC from the perspectives of prognosis, molecular mechanism and regulatory mode.…”

Section: Discussionmentioning

confidence: 99%

The effect of a novel glycolysis-related gene signature on progression, prognosis and immune microenvironment of renal cell carcinoma

Guan

Xue

et al. 2020

BMC Cancer

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Background Glycolysis is a central metabolic pathway for tumor cells. However, the potential roles of glycolysis-related genes in renal cell carcinoma (RCC) have not been investigated. Methods Seven glycolysis-related gene sets were selected from MSigDB and were analyzed through GSEA. Using TCGA database, the glycolysis-related gene signature was constructed. Prognostic analyses were based on the Kaplan–Meier method. The cBioPortal database was employed to perform the mutation analyses. The CIBERSORT algorithm and TIMER database were used to determine the immunological effect of glycolytic gene signature. The expressions in protein level of eight glycolytic risk genes were determined by HPA database. Finally, qPCR, MTT and Transwell invasion assays were conducted to validate the roles of core glycolytic risk genes (CD44, PLOD1 and PLOD2) in RCC. Results Four glycolysis-related gene sets were significantly enriched in RCC samples. The glycolytic risk signature was constructed (including CD44, PLOD2, KIF20A, IDUA, PLOD1, HMMR, DEPDC1 and ANKZF1) and identified as an independent RCC prognostic factor (HR = 1.204). Moreover, genetic alterations of glycolytic risk genes were uncommon in RCC (10.5%) and glycolytic risk signature can partially affect immune microenvironment of RCC. Six glycolytic risk genes (except for IDUA and HMMR) were over-expression in A498 and 786-O renal cancer cells through qPCR test. MTT and Transwell assays revealed that silencing of CD44, PLOD1 and PLOD2 suppressed the proliferation and invasion of renal cancer cells. Conclusions The glycolysis-related risk signature is closely associated with RCC prognosis, progression and immune microenvironment. CD44, PLOD1 and PLOD2 may serve as RCC oncogenes.

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Section: Discussionmentioning

confidence: 99%

The effect of a novel glycolysis-related gene signature on progression, prognosis and immune microenvironment of renal cell carcinoma

Guan

Xue

et al. 2020

BMC Cancer

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“…A newly identified oncogenic lncRNA in renal cancer [ 46 , 47 ], lncRNA Activated in RCC with Sunitinib Resistance ( lncARSR ), is also highly expressed in CRC tissues and predicts poor disease-free survival (DFS) (hazard ratio (HR), 2.484; 95% CI, 1.132–6.232; p = 0.028) and OS (HR, 3.250; 95% CI, 1.596–6.716; p = 0.001). In the molecular context, lncARSR sponges miR-34a-5p and, consequently, enhances hexokinase 1 (HK1)-mediated aerobic glycolysis in vitro and in vivo [ 48 ].…”

Section: Resultsmentioning

confidence: 99%

Involvement of Long Non-Coding RNAs in Glucose Metabolism in Cancer

Balihodzic

Barth

Prinz

et al. 2021

Cancers

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The rapid and uncontrolled proliferation of cancer cells is supported by metabolic reprogramming. Altered glucose metabolism supports cancer growth and progression. Compared with normal cells, cancer cells show increased glucose uptake, aerobic glycolysis and lactate production. Byproducts of adjusted glucose metabolism provide additional benefits supporting hallmark capabilities of cancer cells. Long non-coding RNAs (lncRNAs) are a heterogeneous group of transcripts of more than 200 nucleotides in length. They regulate numerous cellular processes, primarily through physical interaction with other molecules. Dysregulated lncRNAs are involved in all hallmarks of cancer including metabolic alterations. They may upregulate metabolic enzymes, modulate the expression of oncogenic or tumor-suppressive genes and disturb metabolic signaling pathways favoring cancer progression. Thus, lncRNAs are not only potential clinical biomarkers for cancer diagnostics and prediction but also possible therapeutic targets. This review summarizes the lncRNAs involved in cancer glucose metabolism and highlights their underlying molecular mechanisms.

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“…MiR-34a is a mature tumor suppressor miRNA, which has been confirmed in a variety of cancers, such as hepatocellular carcinoma and colorectal cancer [20,21]. Moreover, miR-34a is reported to be frequently downregulated in OC, and the overexpression of miR-34a can inhibit cancer progression by suppressing the expression of many oncogenic genes, such as snail [11,22].…”

Section: Discussionmentioning

confidence: 99%

LncRNA OIP5-AS1 upregulates snail expression by sponging miR-34a to promote ovarian carcinoma cell invasion and migration

Jiang

et al. 2020

Biol Res

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Background Although OIP5-AS1 has been characterized as an oncogenic lncRNA in many types of cancer, its role and underlying mechanism in ovarian carcinoma (OC) remains unknown. This study aimed to investigate the role of OIP5-AS1 in OC. Methods OC tissues and non-tumor tissues (ovary tissues within 3 cm around tumors) were collected from 58 OC patients (age range 36 to 67 years old, mean age 51.4 ± 5.9 years old). The expression of OIP5-AS1 and snail in paired tissues were determined by RT-qPCR. The interaction between OIP5-AS1 and miR-34a was predicted by IntaRNA2.0 and confirmed by dual luciferase reporter assay. The effects of overexpression of OIP5-AS1 and miR-34a on the expression of snail were analyzed by RT-qPCR and Western blotting. Cell invasion and migration were analyzed by Transwell assay. Results We observed that the expression of OIP5-AS1 and snail was upregulated and positively correlated with each other in OC. RNA–RNA interaction analysis showed that OIP5-AS1 might sponge miR-34a. In OC cells, overexpression of OIP5-AS1 resulted in the upregulated expression of snail, while overexpression of miR-34a downregulated the expression of snail. In addition, overexpression of miR-34a reduced the effects of overexpression of OIP5-AS1 on the expression of snail. In cell invasion and migration assay, overexpression of OIP5-AS1 and snail resulted in increased OC cell invasion and migration, while overexpression of miR-34a decreased OC cell invasion and migration. Moreover, overexpression of miR-34a attenuated the effects of OIP5-AS1 overexpression on OC cell invasion and migration. Conclusions Therefore, OIP5-AS1 may upregulate snail expression in OC by sponging miR-34a to promote OC cell invasion and migration.

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lncARSR sponges miR‐34a‐5p to promote colorectal cancer invasion and metastasis via hexokinase‐1‐mediated glycolysis

Cited by 36 publications

References 21 publications

The effect of a novel glycolysis-related gene signature on progression, prognosis and immune microenvironment of renal cell carcinoma

The effect of a novel glycolysis-related gene signature on progression, prognosis and immune microenvironment of renal cell carcinoma

Involvement of Long Non-Coding RNAs in Glucose Metabolism in Cancer

LncRNA OIP5-AS1 upregulates snail expression by sponging miR-34a to promote ovarian carcinoma cell invasion and migration

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