Abstract
Neuroblastoma (NB) is the most common extracranial solid tumor in childhood. Outcome for children with high-risk NB remains unsatisfactory. Accumulating evidence suggests that tripartite motif (TRIM) family proteins express diversely in various human cancers and act as regulators of oncoproteins or tumor suppressor proteins. This review summarizes the TRIM proteins involving in NB and the underlying molecular mechanisms. We expect these new insights will provide important implications for the treatment of NB by targeting TRIM proteins.
Highlights
Neuroblastoma (NB) is the most common extracranial solid tumor in childhood, accounting for 8–10% of all children’s malignancies and about 15% of cancer-related deaths [1,2]
A recent study revealed that TRIM11 regulates the proliferation and apoptosis of breast cancer cells by regulating ERK1/2 and JNK1/2 signaling pathways [29]. These results indicate that TRIM11 is responsible for different oncogenic processes in various cancers
TRIM16 can enhance the transcription of retinoic acid receptor β (RARβ), and overexpression of TRIM16 significantly reduces the proliferation of RA-sensitive NB cells as well as RA-resistant lung and breast cancer cells [42]. These findings suggest an important role of TRIM16 in the response of these tumor cells to differentiating agents, such as RA, an effective inducer of NB cell differentiation that has been used in the clinic for the treatment of high-risk NB [43]
Summary
Neuroblastoma (NB) is the most common extracranial solid tumor in childhood, accounting for 8–10% of all children’s malignancies and about 15% of cancer-related deaths [1,2]. A recent study revealed that TRIM11 regulates the proliferation and apoptosis of breast cancer cells by regulating ERK1/2 and JNK1/2 signaling pathways [29].
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