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. Author manuscript; available in PMC: 2021 Feb 15.
Published in final edited form as: Cancer Res. 2020 Jun 15;80(16):3265–3278. doi: 10.1158/0008-5472.CAN-19-3613

Figure 7. A schematic proposed model of HDAC10 in KRAS-driven lung cancer development.

Figure 7.

Hdac10 deficiency in the presence of oncogenic KRAS accelerates lung tumorigenesis in mice. The loss of HDAC10 induces SOX9 transcription and upregulates CD44 expression in LUAD cells by activating TGF-β signaling. HDAC10 regulates the stem-like properties of tumor cells through the TGF-β/SOX9 pathway.