ArticleOncogene2018
Shared and independent functions of aPKCλ and Par3 in skin tumorigenesis.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- RICH1 enhances pro-inflammatory TAM infiltration in breast cancer via promoting TRIM21-mediated ubiquitination of RhoA and inhibiting STAT3 phosphorylation.NPJ precision oncology · 2025Article
- Integrated profiling reveals polarity protein dysregulation during oral cancer progression.Scientific reports · 2025Article
- High ROR1 Expression Is Associated With Poor Differentiation and Perineural Invasion in Cutaneous Squamous Cell Carcinoma.Experimental dermatology · 2025Article
- Cell polarity proteins promote macropinocytosis in response to metabolic stress.Nature communications · 2024Article
- Cell polarity changes in cancer initiation and progression.The Journal of cell biology · 2024Review
- Polarity in skin development and cancer.Current topics in developmental biology · 2023Article
- Dual Function of Par3 in Tumorigenesis.Frontiers in oncology · 2022Review
- lncRNA NEAT1 Downregulation Ameliorates the Myocardial Infarction of Mice by Regulating the miR-582-5p/F2RL2 Axis.Cardiovascular therapeutics · 2022Article
- Orchestration of tissue-scale mechanics and fate decisions by polarity signalling.The EMBO journal · 2021Review
- The polarity protein PARD3 and cancer.Oncogene · 2021Review
- RAS-mediated suppression of PAR3 and its effects on SCC initiation and tissue architecture occur independently of hyperplasia.Journal of cell science · 2020Article
- Polarity signaling ensures epidermal homeostasis by coupling cellular mechanics and genomic integrity.Nature communications · 2019Article
- Epithelial polarity limits EMT.Nature cell biology · 2019Article
- Polarity protein Canoe mediates overproliferation via modulation of JNK, Ras-MAPK and Hippo signalling.Cell proliferation · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The polarity proteins Par3 and aPKC are key regulators of processes altered in cancer. Par3/aPKC are thought to dynamically interact with Par6 but increasing evidence suggests that aPKC and Par3 also exert complex-independent functions. Whereas aPKCλ serves as tumor promotor, Par3 can either promote or suppress tumorigenesis. Here we asked whether and how Par3 and aPKCλ genetically interact to control two-stage skin carcinogenesis. Epidermal loss of Par3, aPKCλ, or both, strongly reduced tumor multiplicity and increased latency but inhibited invasion to similar extents, indicating that Par3 and aPKCλ function as a complex to promote tumorigenesis. Molecularly, Par3/aPKCλ cooperate to promote Akt, ERK and NF-κB signaling during tumor initiation to sustain growth, whereas aPKCλ dominates in promoting survival. In the inflammatory tumorigenesis phase Par3/aPKCλ cooperate to drive Stat3 activation and hyperproliferation. Unexpectedly, the reduced inflammatory signaling did not alter carcinogen-induced immune cell numbers but reduced IL-4 Receptor-positive stromal macrophage numbers in all mutant mice, suggesting that epidermal aPKCλ and Par3 promote a tumor-permissive environment. Importantly, aPKCλ also serves a distinct, carcinogen-independent role in controlling skin immune cell homeostasis. Collectively, our data demonstrates that Par3 and aPKCλ cooperate to promote skin tumor initiation and progression, likely through sustaining growth, survival, and inflammatory signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.