2023
DOI: 10.1016/j.bbadis.2023.166817
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Physical interaction between STAT3 and AP1 in cervical carcinogenesis: Implications in HPV transcription control

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Cited by 5 publications
(1 citation statement)
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“…The dashed lines indicate the proposed action of STAT3 in HPV-positive cancer cells: STAT3 has been reported to increase HPV E6/E7 oncogene expression through a mechanism that may not require direct binding of STAT3 to the viral transcriptional control region (upstream regulatory region, URR). 18,65 Further, STAT3 signaling has been described to be stimulated by an E6-dependent induction of an IL-6-linked autocrine loop 15 and by phosphorylation through JAK2. 51 Experimental tools employed in this study to negatively regulate STAT3 or HPV E6/E7 are indicated in red (chemical JAK and STAT3 inhibitors, CPX, siRNAs, CRISPR/Cas9), tools to increase STAT3 activities are depicted in green (OSM, STAT3 overexpression).…”
Section: Author Contributionsmentioning
confidence: 99%
“…The dashed lines indicate the proposed action of STAT3 in HPV-positive cancer cells: STAT3 has been reported to increase HPV E6/E7 oncogene expression through a mechanism that may not require direct binding of STAT3 to the viral transcriptional control region (upstream regulatory region, URR). 18,65 Further, STAT3 signaling has been described to be stimulated by an E6-dependent induction of an IL-6-linked autocrine loop 15 and by phosphorylation through JAK2. 51 Experimental tools employed in this study to negatively regulate STAT3 or HPV E6/E7 are indicated in red (chemical JAK and STAT3 inhibitors, CPX, siRNAs, CRISPR/Cas9), tools to increase STAT3 activities are depicted in green (OSM, STAT3 overexpression).…”
Section: Author Contributionsmentioning
confidence: 99%