IndraLab

Statements


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"XREF_BIBR used T83 (a new 4-arylidene curcumin analogue) to inhibit the expression of Jab1 in NPC cells, demonstrating that inhibition of Jab1 could reduce tumor cell growth, induce G 2 / M arrest, and increase tumor cell apoptosis, thus enhancing the sensitivities of NPC cells to radiotherapy."

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"In HCC, abnormal expression of JAB1 can significantly reduce CDKN1C and p57 levels and promote tumor cell growth."

eidos
"JAB1 promoted ESCC cell growth The CCK-8 assay revealed that the Eca109 and EC9706 cells transfected with the JAB1 overexpression lentivirus showed significantly increased absorbance compared to normal cells , ( Fig 3a ) ."

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"Experiments showing that the knock-down of p8 expression results in a strong inhibition of Jab1 activity confirmed that the mechanism by which Jab1 promotes cell growth by decreasing p27 level is p8 dependent."

eidos
"Similar to AR-positive PC cells , inhibition of CSN5 repressed cell growth ( Fig. 4A ) ."

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"Our group recently found that Jab1 contributes to NPC tumorigenesis and resistance to radiotherapy by promoting NPC cell growth, dysregulating NPC cell cycle progression, and inhibiting radiation induced apoptosis XREF_BIBR, XREF_BIBR, XREF_BIBR."

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"Jab1 and CSN5 promotes NPC cell growth."

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"We also found that knockdown of CSN5 remarkably suppressed cell growth by inducing cell cycle arrest and apoptosis promotion in NSCLC cells."

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"Knockdown of COPS5 and COPS6 inhibited cell growth and migration of the CAL27 and SCC25 cell lines."