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The p75^NTR and its carboxyl-terminal fragment exert opposing effects on melanoma cell proliferation and apoptosis via modulation of the NF-κB pathway.

ABSTRACT: The p75 neurotrophin receptor (p75^NTR ), a member of the tumor necrosis factor superfamily of receptors, is sensitive to proteolysis and has been observed to be expressed in various cancers. However, the roles of p75^NTR and its proteolytic fragments in tumorigenesis remain incompletely understood. Here, we report that the proportion of the p75^NTR carboxyl-terminal fragment (p75^NTR -CTF) is much higher than that of the full-length p75^NTR (p75^NTR -FL) in melanoma cells. Whereas p75^NTR -FL positively regulates apoptosis, p75^NTR -CTF promotes cell proliferation and survival, as well as increasing sorafenib resistance in vivo and in vitro. Moreover, p75^NTR -CTF activates the nuclear factor kappa B

SUBMITTER: Zhong M

PROVIDER: S-EPMC7780107 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

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Dataset Information

The p75^NTR and its carboxyl-terminal fragment exert opposing effects on melanoma cell proliferation and apoptosis via modulation of the NF-κB pathway.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

The p75NTR and its carboxyl-terminal fragment exert opposing effects on melanoma cell proliferation and apoptosis via modulation of the NF-κB pathway.

OmicsDI is part of the ELIXIR infrastructure

Tweets

The p75^NTR and its carboxyl-terminal fragment exert opposing effects on melanoma cell proliferation and apoptosis via modulation of the NF-κB pathway.