Background: Mitophagy is a mitochondrial quality-control pathway whose contribution to cancer stress tolerance may vary by cellular context. For essential oils, mechanistic interpretation is often limited by compositional variability and the limited number of studies addressing malignant and non-malignant comparisons under matched exposure conditions. Methods: Ylang Ylang essential oil (YY EO) was characterized by GC-MS-FID. Lung cancer cells (A549) and a salivary gland carcinoma model (HTB-41), together with non-malignant lung-related cells (BEAS-2B, MRC-5), were exposed to YY EO. Functional outcomes were assessed by WST-1 and LDH assays. Mitophagy-related and mitochondrial quality-control-associated genes were quantified by RT-qPCR (2^−ΔΔCt). Results: GC-MS-FID identified a terpenoid-rich mixture (99.31%), with germacrene D and β-caryophyllene among the major constituents. YY EO was associated with dose- and cell-type-dependent functional responses, with malignant cells showing reductions in WST-1 signal and stronger LDH-associated responses under the tested conditions, while non-malignant cells showed less pronounced functional changes. Transcriptional responses were context-dependent, with differential changes in mitophagy-related genes across cell lines. Conclusions: These findings provide comparative evidence of greater functional sensitivity in malignant cells, alongside cell-context-dependent mitophagy-related transcriptional responses. These observations are hypothesis-generating and remain limited to functional readouts and mRNA-level data. Within these limits, the present study provides a composition-anchored comparative dataset that may support future mechanistic studies in this area.

Background/Objectives: Drug resistance is a major challenge in cancer therapy, and mitochondria contribute to this process by controlling both metabolic adaptability and cell survival signaling. Mitophagy, the selective lysosomal removal of dysfunctional mitochondria, has been implicated in therapy resistance, yet its role in sunitinib-resistant renal cancer remains poorly defined. Methods: In this study, acquired sunitinib resistance was established in ACHN renal cancer cells through eight months of stepwise dose escalation. Initial selection conditions were determined using CCK-8 viability and crystal violet colony assays in parental ACHN cells, whereas sustained proliferation under continuous sunitinib exposure was used as the operational criterion for the resistant phenotype. Resistant and parental sensitive cells were treated with 25 µM and 50 µM succinic acid, alone or in combination with sunitinib. Gene expression of BNIP3, NIX, FUNDC1, LC3, PINK1, Parkin, PGAM5, SRC, LONP1, and ATP5F1A was measured by RT-qPCR, and BNIP3 and NIX protein levels were assessed by ELISA. Results: Resistant cells showed significant upregulation of receptor-mediated mitophagy components BNIP3, NIX and FUNDC1 (p < 0.05), with no significant change in LC3, alongside suppression of PINK1, Parkin, and mitochondrial homeostasis-associated genes LONP1, PGAM5, and ATP5F1A (p < 0.05). Succinic acid predominantly reduced BNIP3 and NIX protein levels in both cell lines and suppressed BNIP3, NIX, and LC3 mRNA expression in resistant cells. In contrast, the sunitinib + 50 µM succinic acid combination selectively increased PARKIN, PGAM5, LONP1, and ATP5F1A expression in resistant cells (2.49- to 5.98-fold; p < 0.005), a pattern not observed in parental cells. Conclusions: These findings indicate that sunitinib resistance in ACHN cells is associated with upregulated transcription of receptor-mediated mitophagy components and downregulated transcription of PINK1/Parkin pathway genes, and that exogenous succinic acid selectively upregulates PARKIN and other mitochondrial homeostasis-related gene expression in resistant, but not parental, cells.

The biological basis of suicidal behavior extends beyond psychiatric diagnosis, and alterations in stress-response regulation, monoaminergic signaling, and GABAergic function may contribute to suicide risk. We enrolled 69 adults presenting to the emergency department after a suicide attempt episode and 72 controls. Expression of eight candidate genes (SLC6A3, SLC6A4, NR3C1, NR3C2, DRD2, MAOA, GABRA2, and GABBR2) was measured by qRT-PCR in paired peripheral blood and buccal swab samples, with GAPDH as the reference gene. Multiple testing was addressed with the Benjamini—Hochberg false discovery rate. NR3C2, which encodes the mineralocorticoid receptor, was the only gene downregulated in both sample types after FDR correction (blood: q = 0.0007; swab: q = 0.0004). Blood additionally showed changes in SLC6A4 (↓), DRD2 (↑), and GABBR2 (↑). In buccal swabs, every gene that reached significance—SLC6A3, NR3C1, GABRA2, and GABBR2—was downregulated. No gene achieved AUC ≥ 0.90 in ROC analysis. Gene-by-biochemistry correlations did not survive FDR correction, suggesting transcriptional changes independent of acute metabolic status. Overall, peripheral expression was matrix-dependent, and NR3C2 downregulation stood out as the one signal that replicated across both. Blood and buccal swabs captured complementary biological information, together pointing to impaired HPA-axis buffering. Because group-level confounders could not be adjusted for, these findings should be read as hypothesis-generating and warrant confounder-controlled, longitudinal validation.