Panoply™ Human TYK2 Knockdown Stable Cell Line

Esophageal squamous cell carcinoma (ESCC) is an aggressive and highly fatal malignant tumor with a low five-year survival rate. Identifying new therapeutic targets and their inhibitors is crucial for the prevention and treatment of ESCC. Here, studies show that TYK2 is highly expressed in ESCC and acts as an oncogene. Cirsiliol can bind to TYK2 and inhibit its activity, thereby reducing the dimerization and nuclear localization of signal transducer and activator of transcription 3 (STAT3). Cirsiliol inhibits ESCC growth both in vitro and in vivo. TYK2 is a potential therapeutic target for ESCC, and cirsiliol can inhibit the development and progression of ESCC by inhibiting TYK2.

To evaluate the role of TYK2 in esophageal squamous cell carcinoma (ESCC), researchers examined the protein levels of TYK2 in immortalized esophagus cell SHEE and ESCC cell lines. The results showed that TYK2 protein levels were higher in ESCC cell lines than in immortalized esophageal cells (Figure 1a, upper panel). Subsequently, researchers constructed TYK2 knockdown KYSE140 and KYSE450 cell lines, both of which exhibited high TYK2 expression (Figure 1a). The study demonstrated that the growth of TYK2-knockdown KYSE140 and KYSE450 cells was inhibited (Figure 1b). Similarly, anchorage-independent cell growth was also reduced in the TYK2-knockdown cell group (Figure 1c). Furthermore, tumor growth in cell-derived xenograft (CDX) mouse models was also reduced after TYK2 knockdown (Figure 1d and 1e), and the average tumor weight in the TYK2-knockdown group was lower than that in the control group (Figure 1f). The cell cycle of both TYK2-knockdown KYSE140 and KYSE450 cell lines was arrested at the G2/M phase. Similarly, the migration ability of KYSE140 and KYSE450 cells was also reduced after TYK2 knockdown.

Figure 1. TYK2 knockdown suppresses ESCC growth. (Jia X, et al., 2021)