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Solute carrier family members control essential physiological functions and are tightly linked to human diseases. Solute carrier family 35 member F2 ( SLC 35F2) is aberrantly activated in several malignancies. However, the biological function and molecular mechanism of  SLC 35F2 in papillary thyroid carcinoma ( PTC ) are yet to be fully explored. Here, we showed that  SLC 35F2 was prominently upregulated in  PTC  tissues at both protein and  mRNA  expression level compared with matched adjacent normal tissues. Besides, the high expression of  SLC 35F2 was significantly associated with lymph node metastasis in patients with  PTC .  CRISPR /Cas9‐mediated knockout of  SLC 35F2 attenuated the tumorigenic properties of  PTC , including cell proliferation, migration and invasion and induced G1 phase arrest. In contrast, ectopic expression of  SLC 35F2 brought about aggressive malignant phenotypes of  PTC  cells. Moreover,  SLC 35F2 expedited the proliferation and migration of  PTC  cells by targeting transforming growth factor‐β type I receptor ( TGFBR 1) and phosphorylation of apoptosis signal‐regulating kinase 1 (p‐ASK‐1), thereby activating the mitogen‐activated protein kinase signaling pathway. The malignant behaviors induced by overexpression of  SLC 35F2 could be abrogated by silencing of  TGFBR 1 using a specific inhibitor. We conducted the first study on  SLC 35F2 in thyroid cancer with the aim of elucidating the functional significance and molecular mechanism of  SLC 35F2. Our findings suggest that  SLC 35F2 exerts its oncogenic effect on  PTC  progression through the mitogen‐activated protein kinase pathway, with dependence on activation of  TGFBR ‐1 and apoptosis signal‐regulating kinase 1.

cancer science

Solute carrier family 35 member F2 is indispensable for papillary thyroid carcinoma progression through activation of transforming growth factor‐β type I receptor/apoptosis signal‐regulating kinase 1/mitogen‐activated protein kinase signaling axis