TESC, also known as tescalcin, is a calcium-binding EF hand protein that plays crucial roles in chromatin remodeling, transcriptional regulation, and epigenetic modifications [4]. It is involved in multiple biological processes including cell differentiation and growth, and is associated with various signaling pathways such as EGFR-STAT3, ERK, and AKT [1,2,3].

In cancer research, knockdown of TESC via RNA interference has shown significant effects. In cholangiocarcinoma, TESC knockdown suppresses tumor growth, decreases the level of FOXM1 leading to cell cycle arrest, and attenuates TGF-α-induced tumor cell proliferation in vivo [1]. In differentiated thyroid cancer, reducing TESC expression inhibits cell proliferation, migration, and invasion, downregulates EMT pathway markers, and increases iodine uptake [2]. In esophageal squamous carcinoma, TESC knockdown inhibits tumor cell proliferation, invasion, migration, and EMT progression, and suppresses the growth of carcinoma in vivo [3]. In liver cancer, TESC is associated with poor prognosis, and its knockdown may impact cancer stem cell properties [4]. In papillary thyroid microcarcinoma, TESC knockdown affects the expression of c-Fos related to the ERK signaling pathway, inhibiting tumor growth and metastasis [5].

In conclusion, TESC is a significant gene involved in cell growth-related biological processes. Research using loss-of-function models, mainly RNA interference-mediated knockdown, has revealed its oncogenic roles in multiple cancers, including cholangiocarcinoma, thyroid cancer, esophageal squamous carcinoma, and liver cancer. These findings provide potential targets for cancer diagnosis and treatment.