HOTAIR/miR-326/FUT6 axis facilitates colorectal cancer progression through regulating fucosylation of CD44 via PI3K/AKT/mTOR pathway

Pan, Shimeng; Li, Yanqiu; Liu, Qianqian; Xiao, Yang; Liu, Bing; Ren, Xiang; Qi, Xia; Zhou, Huimin; Chang-qian, Zeng; Li, Jia

doi:10.1016/j.bbamcr.2019.02.004

Cited by 70 publications

(48 citation statements)

References 24 publications

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“…The theory of ceRNA has attracted great attention recently, wherein miRNAs are sequestered by lncRNAs that serve as molecular sponges to affect gene expression ultimately (Li, Zhang, et al, 2017). For instance, HOTAIR/miR-326/FUT6 axis promotes CRC development (Pan et al, 2019 was sponged by lncRNAs in the progression of cancers (Jia et al, 2016;Santos et al, 2017). Likewise, we discovered that MAGI2-AS3 could bind with miR-3163 and negatively regulated miR-3163.…”

Section: Discussionmentioning

confidence: 91%

“…The theory of ceRNA has attracted great attention recently, wherein miRNAs are sequestered by lncRNAs that serve as molecular sponges to affect gene expression ultimately (Li, Zhang, et al, ). For instance, HOTAIR/miR‐326/FUT6 axis promotes CRC development (Pan et al, ). LINC00511 induced by SP1 drives the glioma development via miR‐124‐3p/CCND2 axis (Song, Yuan, Li, Ma, & Sun, ).…”

Section: Discussionmentioning

confidence: 99%

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Long noncoding MAGI2‐AS3 promotes colorectal cancer progression through regulating miR‐3163/TMEM106B axis

Ren

Zheng-jun

et al. 2019

Journal Cellular Physiology

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Colorectal cancer (CRC), is mostly derived from normal colon epithelial cells, and has been reported to be one of most common gastrointestinal malignancies globally. An increasing number of researchers have claimed that long noncoding RNAs (lncRNAs) exert significant functions in tumor progression. Nevertheless, the function of MAGI2-AS3 remains uncertain in CRC. The expression of MAGI2-AS3, miR-3163, and transmembrane protein 106B (TMEM106B) messenger RNA was examined by quantitative real-time polymerase chain reaction. Cell apoptosis was measured by caspase-3 activity test. Cell proliferation was tested by cell-counting kit 8 and 5-ethynyl-2′-deoxyuridine assays. Cell migration was detected by transwell assay. Western blot analysis examined the protein expression of TMEM106B. The expression of Ki-67 was evaluated by immunohistochemistry assay. The binding capacity between miR-3163 and MAGI2-AS3 (or TMEM106B) was studied by radioimmunoprecipitation and luciferase reporter assays. The expression of MAGI2-AS3 and TMEM106B was conspicuously upregulated whereas miR-3163 presented lower expression in CRC cells. MAGI2-AS3 deficiency facilitated cell apoptosis but hampered cell proliferation and migration. MAGI2-AS3 combined with miR-3163 and negatively regulated miR-3163 expression. In addition, the administration of sh-MAGI2-AS3 or miR-3163 mimics suppressed CRC cell growth in vivo. Subsequently, miR-3163 targeted TMEM106B and the transfection of sh-MAGI2-AS3 or miR-3163 mimics downregulated TMEM106B expression. Rescue assays verified that TMEM106B overexpression recovered the effects of MAGI2-AS3 inhibition on cell apoptosis, proliferation, and migration in CRC. MAGI2-AS3 drives CRC progression through regulating miR-3163/TMEM106B axis. This supplies innovative insights on the investigation of molecular mechanism in CRC progression. K E Y W O R D S CRC, MAGI2-AS3, miR-3163, TMEM106B

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Section: Discussionmentioning

confidence: 91%

“…The theory of ceRNA has attracted great attention recently, wherein miRNAs are sequestered by lncRNAs that serve as molecular sponges to affect gene expression ultimately (Li, Zhang, et al, ). For instance, HOTAIR/miR‐326/FUT6 axis promotes CRC development (Pan et al, ). LINC00511 induced by SP1 drives the glioma development via miR‐124‐3p/CCND2 axis (Song, Yuan, Li, Ma, & Sun, ).…”

Section: Discussionmentioning

confidence: 99%

Long noncoding MAGI2‐AS3 promotes colorectal cancer progression through regulating miR‐3163/TMEM106B axis

Ren

Zheng-jun

et al. 2019

Journal Cellular Physiology

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“…LncRNA PCAT6 modulates 5-uorouracil chemoresistance in CRC cells through a miR-204/HMGA2 pathway [22]. LncRNA HOTAIR expression is associated with the aggressive biological behaviors of CRC cells [23]. In our research, we found that LINC00342 was up-regulated in CRC.…”

Section: Discussionmentioning

confidence: 50%

LncRNA LINC00342 contributes to the growth and metastasis of colorectal cancer via targeting miR-19a-3p/NPEPL1

Shen

Wang

et al. 2020

Preprint

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Background Long intergenic non-protein coding RNA 00342 (LINC00342) has been identified as a novel oncogene. However, the functional role of LINC00342 in colorectal cancer (CRC) remains unclear. Methods The expression of LINC00342 is detected by real-time PCR (RT-PCR) analysis. Cell proliferation, migration and invasion and xenograft model are examined to analyze the biological functions of LINC00342 in vitro and in vivo using colony formation, would healing and transwell analyses. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays are used to identify the target interactions between LINC00342, miR-19a-3p and aminopeptidase like 1 (NPEPL1). Results LINC00342 was highly expressed in CRC. Down-regulation of LINC00342 inhibited cell proliferation and metastasis of CRC cells. Moreover, knocking down LINC00342 inhibited the tumor growth in vivo. Mechanistic investigation revealed that LINC00342 might sponge miR-19a-3p to regulate NPEPL1 expression. Further investigation indicated that the ontogenesis facilitated by LINC00342 was inhibited due to the depletion of NPEPL1.Conclusion LINC00342 promotes CRC progression by competitively binding miR-19a-3p with NPEPL1.

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Section: Discussionmentioning

confidence: 50%

LncRNA LINC00342 contributes to the growth and metastasis of colorectal cancer via targeting miR-19a-3p/NPEPL1

Shen

Wang

et al. 2020

Preprint

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Background Long intergenic non-protein coding RNA 00342 (LINC00342) has been identified as a novel oncogene. However, the functional role of LINC00342 in colorectal cancer (CRC) remains unclear. Methods The expression of LINC00342 was detected by real-time PCR. Cell proliferation, migration and invasion and xenograft model were examined to analyze the biological functions of LINC00342 in vitro and in vivo. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to identify the target interactions between LINC00342, miR-19a-3p and aminopeptidase like 1 (NPEPL1). Results LINC00342 was highly expressed in CRC. Downregulation of LINC00342 inhibited cell proliferation and metastasis of CRC cells. Moreover, knocking down LINC00342 could weaken the tumor growth in vivo. Mechanistic investigation revealed that LINC00342 might sponge miR-19a-3p to regulate NPEPL1 expression. Further investigation indicated that the oncogenesis facilitated by LINC00342 was inhibited due to the depletion of NPEPL1.Conclusion LINC00342 promoted CRC progression by competitively binding miR-19a-3p with NPEPL1.

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HOTAIR/miR-326/FUT6 axis facilitates colorectal cancer progression through regulating fucosylation of CD44 via PI3K/AKT/mTOR pathway

Cited by 70 publications

References 24 publications

Long noncoding MAGI2‐AS3 promotes colorectal cancer progression through regulating miR‐3163/TMEM106B axis

Long noncoding MAGI2‐AS3 promotes colorectal cancer progression through regulating miR‐3163/TMEM106B axis

LncRNA LINC00342 contributes to the growth and metastasis of colorectal cancer via targeting miR-19a-3p/NPEPL1

LncRNA LINC00342 contributes to the growth and metastasis of colorectal cancer via targeting miR-19a-3p/NPEPL1

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