Perilla / JNK Cancer Research Results

Per, Perilla: Click to Expand ⟱
Features:
Perilla (commonly Perilla frutescens) is an herb used traditionally in various Asian cuisines and traditional medicine. It contains several bioactive compounds including flavonoids, phenolic acids, and fatty acids, which have been studied for their antioxidant, anti-inflammatory, and antimicrobial properties.
Perilla (Perilla frutescens) is an herb used as food and traditional medicine. Mechanistically it’s best treated as a polyphenol-rich extract, often characterized by rosmarinic acid (plus luteolin/apigenin-class flavonoids depending on preparation). In cancer models, perilla extracts and rosmarinic acid–rich fractions are most consistently associated with anti-inflammatory signaling (NF-κB↓), Nrf2/antioxidant activation in normal tissues, and downstream cell-cycle/apoptosis modulation that is generally moderate and model-dependent.

Active fractions (context-dependent): Rosmarinic acid–rich polyphenols (often dominant), plus flavones/flavonoids (luteolin/apigenin-class depending on extract). Effects vary strongly by preparation (leaf vs seed; aqueous vs ethanol; standardized vs crude).

Rank Pathway / Axis Cancer / Tumor Context Normal Tissue Context TSF Primary Effect Notes / Interpretation
1 NF-κB inflammatory signaling NF-κB ↓; COX-2, IL-6, TNF-α ↓ (reported) Inflammation tone ↓ R, G Anti-inflammatory / anti-survival modulation Most consistent mechanistic theme for perilla and rosmarinic-acid–rich fractions.
2 Nrf2 / ARE antioxidant response Context-dependent modulation Nrf2 ↑; HO-1 ↑; GSH systems ↑ R, G Redox buffering Common polyphenol signature; tumor implications vary and may affect therapy sensitivity in some contexts.
3 ROS / redox modulation ROS ↓ (often) or variable; pro-oxidant effects not dominant Oxidative stress ↓ (protective) P, R Antioxidant-leaning redox modulation Perilla is typically antioxidant in inflammatory/oxidative injury models; tumor cytotoxicity is usually weaker than strong pro-oxidants.
4 MAPK pathways (ERK / JNK / p38) MAPK modulation (context-dependent) ↔ P, R, G Signal reprogramming Direction varies with extract composition and cell line; often downstream of redox/inflammation shifts.
5 PI3K → AKT (± mTOR) PI3K/AKT ↓ (reported; model-dependent) ↔ R, G Growth/survival modulation Often secondary to NF-κB and oxidative stress pathway changes.
6 Cell-cycle arrest (G1 / G2-M) Cell-cycle arrest ↑ (reported; modest) ↔ G Cytostasis Phenotype-level effect; strength depends on dose and extract standardization.
7 Intrinsic apoptosis (mitochondrial) Apoptosis ↑ (reported; modest); caspases ↑ ↔ (limited activation) G Conditional cytotoxicity Usually not a “direct toxin” signature; more consistent as an anti-inflammatory/antioxidant modulator.
8 Angiogenesis signaling (VEGF) VEGF ↓ (reported in some systems) ↔ G Anti-angiogenic modulation Evidence exists but is less consistent than NF-κB/Nrf2 effects.
9 Invasion / metastasis (MMPs / EMT) MMP2/MMP9 ↓; migration ↓ (reported) ↔ G Anti-invasive phenotype Often downstream of NF-κB and MAPK modulation; not universal across models.
10 Extract variability / bioavailability constraint Activity varies by part (leaf/seed), solvent, and standardization — — Translation constraint Perilla is best treated as “rosmarinic-rich polyphenol extract”; systemic exposure may not match in-vitro doses.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (rapid redox interactions)
  • R: 30 min–3 hr (acute transcription/signaling shifts)
  • G: >3 hr (gene-regulatory and phenotype-level outcomes)
JNK, c-Jun N-terminal kinase (JNK): Click to Expand ⟱
Source:
Type:
JNK acts synergistically with NF-κB, JAK/STAT, and other signaling molecules to exert a survival function. Janus signaling promotes cancer cell survival.
JNK, or c-Jun N-terminal kinase, is a member of the mitogen-activated protein kinase (MAPK) family. It plays a crucial role in various cellular processes, including cell proliferation, differentiation, and apoptosis (programmed cell death). JNK is activated in response to various stress signals, such as UV radiation, oxidative stress, and inflammatory cytokines.
JNK activation can promote apoptosis in cancer cells, acting as a tumor suppressor. However, in other contexts, it can promote cell survival and proliferation, contributing to tumor progression.

JNK is often unregulated in cancers, leading to increased cancer cell proliferation, survival, and resistance to apoptosis. This activation is typically associated with poor prognosis and aggressive tumor behavior.
Scientific Papers found: Click to Expand⟱
3017- RosA,  Per,    Molecular Mechanism of Antioxidant and Anti-Inflammatory Effects of Omega-3 Fatty Acids in Perilla Seed Oil and Rosmarinic Acid Rich Fraction Extracted from Perilla Seed Meal on TNF-α Induced A549 Lung Adenocarcinoma Cells
- in-vitro, Lung, A549
TumCD∅, ROS↓, IL1β↓, IL6↓, IL8↓, TNF-α↓, COX2↓, SOD2↓, FOXO1↓, NF-kB↓, JNK↓, antiOx↑, tumCV∅,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ROS↓, 1,   SOD2↓, 1,  

Cell Death ⓘ

JNK↓, 1,   TumCD∅, 1,  

Transcription & Epigenetics ⓘ

tumCV∅, 1,  

Proliferation, Differentiation & Cell State ⓘ

FOXO1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL1β↓, 1,   IL6↓, 1,   IL8↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  
Total Targets: 14

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: JNK, c-Jun N-terminal kinase (JNK)
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:336  Target#:168  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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