&lt;p&gt;Long Non-Coding RNA AC118344.1 Promotes Gastric Cancer Cell Proliferation, Invasion, and Metastasis via AKT2 and Its Downstream Molecules HK2 and MMP2&lt;/p&gt;

Liang, Cai; Xue, Yangji; Ding, Jianzu; Zheng, Bin

doi:10.2147/cmar.s281608

Cited by 1 publication

(1 citation statement)

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“…18 Several lncRNAs are known to function via this mechanism in GC cells including PTCSC3, MALAT1, AC118344.1, LINC00689, and p4516. [19][20][21][22][23] We similarly explore the function of MAGI1-IT1 as a ceRNA and determined that it was predicted to bind to miR-302d-3p, which is a miRNA that has previously been shown to suppress cervical squamous cell carcinoma tumor growth. 13 We confirmed the ability of MAGI1-IT1 to sequester miR- Importantly, miR-302d-3p inhibition was sufficient to reverse the impacts of MAGI1-IT1 knockdown on GC cell proliferation, confirming that MAGI1-IT1 regulates…”

Section: Discussionmentioning

confidence: 99%

The Long Noncoding RNA MAGI1-IT1 Regulates the miR-302d-3p/IGF1 Axis to Control Gastric Cancer Cell Proliferation

Wang¹,

Gu²,

Zhuang³

et al. 2021

CMAR

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Background: MAGI1-IT1 is a long non-coding RNA (lncRNA) previously reported to regulate several cancer types, but its functional role in gastric cancer (GC) remains to be defined. This study therefore explored the mechanistic role played by MAGI1-IT1 in the regulation of GC cell proliferation. Methods: 120 pairs of GC patient tumor, paracancerous tissues, human GES-1 control cells and human AGS, MKN-74, MKN-45, and MGC-803 GC cell lines were used to detected MAGI1-IT1, miR-302d-3p, and IGF1 expression by a qPCR approach. An shRNA approach was used to knock down MGI1-IT1 in order to examine the effect of such treatment on GC cell proliferation, and rescue experiments were subsequently conducted. In addition, the functional role of MAGI1-IT1 in GC in vivo was evaluated with a xenograft model system. P < 0.05 was the significance threshold. Results: Elevated MAGI1-IT1 expression was detected in GC cell lines and tissues, and was linked to poorer patient overall survival. Knocking down this lncRNA disrupted GC cell proliferation in vitro and in vivo, and miR-302d-3p was identified as a MAGI1-IT1 target. Notably, miR-302d-3p inhibition partially reversed the impact of MAGI1-IT1 knockdown on GC cell proliferation. IGF1 was subsequently identified as a miR-302d-3p target gene that was upregulated by MAGI1-IT1 through miR-302d-3p. Conclusion: Overall, these results indicated that MAGI1-IT1 controlled GC cell proliferation by modulating the miR-302d-3p/IGF1 axis, suggesting that this may be a viable treatment target in those with GC.

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