TY - JOUR
T1 - Reciprocal regulation of signaling and endocytosis
T2 - Implications for the evolving cancer cell
AU - Schmid, Sandra L.
N1 - Funding Information:
I am grateful to Dr. Marcel Mettlen for illustrations, all Schmid laboratory members for helpful discussions, and to this paper’s referee, who provided helpful comments and discussions that greatly improved the review. Boning Gao performed the analyses of dynamin expression in normal and cancer-derived lung cells. Several colleagues at University of Texas Southwestern also provided helpful comments on the manuscript, including Maralice Conacci-Sorrell, Joe Goldstein, Mike Henne, Jim Malter, David Russell, and Jerry Shay. Research in the Schmid laboratory was supported by National Institutes of Health R01 grants GM42455, GM73165 (with G. Da-nuser), and MH61345, as well as by Cancer Prevention and Research Institute of Texas grant RP150573 and Welch Foundation grant I-1823. The author declares no competing financial interests.
Publisher Copyright:
© 2017 Schmid.
PY - 2017/9/1
Y1 - 2017/9/1
N2 - Cell surface receptor uptake via clathrin-mediated endocytosis (CME) and subsequent intracellular sorting for degradation or recycling regulates the strength and specificity of downstream signaling. Signaling, in turn, modulates early endocytic trafficking. This reciprocal regulation of signaling and endocytosis provides opportunities for the establishment of feedback loops to enhance or suppress surface-derived signals. Recent studies suggest that dynamin-1, a presumed neuron-specific isoform of the large, membrane fission GTPase, can be activated in nonneuronal cells downstream of cancer-relevant signaling pathways and thereby function as a nexus between signaling and early endocytic trafficking. I speculate that sustained up-regulation and/or acute activation of dynamin-1 in cancer cells contributes to a program of "adaptive" CME that alters signaling to enhance cancer cell survival, migration, and proliferation.
AB - Cell surface receptor uptake via clathrin-mediated endocytosis (CME) and subsequent intracellular sorting for degradation or recycling regulates the strength and specificity of downstream signaling. Signaling, in turn, modulates early endocytic trafficking. This reciprocal regulation of signaling and endocytosis provides opportunities for the establishment of feedback loops to enhance or suppress surface-derived signals. Recent studies suggest that dynamin-1, a presumed neuron-specific isoform of the large, membrane fission GTPase, can be activated in nonneuronal cells downstream of cancer-relevant signaling pathways and thereby function as a nexus between signaling and early endocytic trafficking. I speculate that sustained up-regulation and/or acute activation of dynamin-1 in cancer cells contributes to a program of "adaptive" CME that alters signaling to enhance cancer cell survival, migration, and proliferation.
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U2 - 10.1083/jcb.201705017
DO - 10.1083/jcb.201705017
M3 - Article
C2 - 28674108
AN - SCOPUS:85028853452
SN - 0021-9525
VL - 216
SP - 2623
EP - 2632
JO - Journal of Cell Biology
JF - Journal of Cell Biology
IS - 9
ER -