IndraLab

Statements



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"Conclusions : Eag1 may promote osteosarcoma cell proliferation and invasion by targeting STAT3-VEGF pathway and may be a potential therapeutic target for osteosarcoma."

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"Kv10.1 also aids cell cycle progression by stabilizing the membrane potential in the G1 phase and enhances invasiveness by modulating focal adhesions (Hartung, 2011)."

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"The results demonstrated that Eag1 siRNAs lead to reduced adhesion, migration, and invasion of MG-63 and Saos-2 cells."

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"The inhibition of Kv10.1 expression can up-regulate miR-126, thereby reducing the invasiveness of BC cells (20)."

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"On the other hand, Eag1 has also been shown to promote the migration and invasion of tumor cells via promoting the formation of pseudopodia (50)."

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"We found that KCNH1 knockdown decreased the migration, invasion, and proliferation of RA FLSs ( Fig. 6 A-D)."

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"Finally, we tried to explain the detailed mechanisms by which OS cell adhesion, migration, and invasion are inhibited by specific blockade of Eag1."

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"Circ_0016347 and KCNH1 promoted proliferation, migration, invasion, and glycolysis of OS cells."

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"KCNH1 knockdown reduced proliferation, migration, invasion and expression of MMP-1 and MMP-13 in RA FLSs."

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"Based on the findings in previous studies that potassium voltage gated channel subfamily H member 1 (KCNH1) was overexpressed in osteosarcoma and promoted the proliferation and invasion of osteosarcoma [XREF_BIBR - XREF_BIBR] and on our profile of the miRanda, PITA, RNAhybrid databases to explore the corresponding circRNAs of KCNH1, we speculated that hsa-circ-0016347 may be a potential regulator of osteosarcoma progression."