Plantamajoside modulates the proliferation, stemness, and apoptosis of lung carcinoma via restraining p38MAPK and AKT phosphorylation

Abstract

Background Plantamajoside (PMS), an active anti-inflammatory component and antioxidant derived from Herba Plantaginis , has been reported to exert a suppressive effect in liver cancer in vivo . In this study, we tested the effects of PMS on the metastatic 95D cell line. Methods 95D cells were characterized as most sensitive to PMS across several lung cancer cell lines. Cell viability within 24 h was tested with CCK-8. Different concentrations of PMS (0, 50, 100, and 200 µg/mL) and 5 µg/mL of cisplatin were established for later 24 h treatment. Relative mRNA and protein expression were assessed with PCR and Western blotting. Cell proliferation and stemness were indicated with colony and sphere formation. Cell metastasis was evaluated with wound healing and Transwell. Apoptotic cells and mitochondrial membrane potential were investigated with flow cytometry. Results CCK-8 assay showed PMS to inhibit the viability of 95D cells in a dose-dependent manner. PMS decreased colony formation and inhibited stemness in 95D cells. Invasion and migration were also inhibited. Moreover, PMS induced cell apoptosis, and decreased mitochondrial membrane potential. All of these effects were dose dependent. Interestingly, PMS treatment reduced the protein expression of p-p38 MAPK and p-AKT but not that of p38 MAPK and AKT. Conclusions PMS inhibited proliferation, stemness, and migration, and initiated apoptosis in 95D cells, possibly through p38 MAPK and AKT dephosphorylation and mitochondria dysfunction. These findings support the promise of PMS as a prodrug in lung cancer treatment.

Efficient hydrogenation of cinnamaldehyde to 3-phenylpropanol on Ni/NiS-modified twin Zn0.5Cd0.5S under visible light irradiation

“…This phenomenon is similar to the sacrificial reagent role in the photocatalytic H 2 evolution reaction, such as a TiO 2 semiconductor as a methanol sacrificial reagent 47,48 and a g-C 3 N 4 photocatalyst as a TEOA sacrificial reagent. [49][50][51] Ethanol was oxidized to acetaldehyde during the reaction. During the photocatalytic reaction, photogenerated holes migrate to the liquid-solid interface (Ni/NiS-ZCS and ethanol) to activate ethanol and deprotonate for generating protons (H + ).…”

Phytochemicals, Biological Activities, Molecular Mechanisms, and Future Prospects of Plantago asiatica L.

“…apoptosis in lung cancer via dephosphorylation of MAPK and AKT, as well as mitochondria dysfunction. 127…”

“…The apigenin ( 1 ) and luteolin ( 2 ) down-regulate NF-κB signaling (IKK, IκB, and NF-κB) and PI3K/AKT signaling (PI3K, AKT, and mTOR); activate or inactivate various signaling targets, such as Bcl-2, Bcl-xL, Bax, caspase-3, and caspase-9; and promote mitochondrial-mediated apoptosis, thereby producing anticancer effects. − Strangely, apigenin ( 1 ) can stimulate autophagic cell apoptosis of gastric cancer via inhibition of HIF-1α and Ezh2 under hypoxia conditions . Acteoside ( 27 ) increases the expression of Bax, caspase-3, and caspase-9 and reduces the expression of Bcl-2, cleaved caspase-3, and cleaved caspase-9 to promote tumor cell apoptosis. − In addition, plantamajoside ( 25 ) initiates cell apoptosis in lung cancer via dephosphorylation of MAPK and AKT, as well as mitochondria dysfunction …”

“…123−126 In addition, plantamajoside (25) initiates cell apoptosis in lung cancer via dephosphorylation of MAPK and AKT, as well as mitochondria dysfunction. 127…”

Plantamajoside Alleviates Substantia Nigra Damage in Parkinson’s Disease Mice by Inhibiting HDAC2/MAPK Signaling and Reducing Microglia Polarization

“…Previous studies have shown that PMS has a wide range of biological activities. , A recent study showed that PMS ameliorated lipopolysaccharide-induced acute lung injury by inhibiting NF-κB as well as MAPK activation. , In addition, PMS can inhibit histone deacetylase 2 (HDAC2) activity in vitro and in vivo and attenuate isoproterene-induced cardiac hypertrophy . HDAC2 is an enzyme that removes acetyl groups from lysine residues at the amino-terminal tail of histones . HDAC2 is upregulated in SN microglia in PD and prevents MPTP-induced loss of SN dopaminergic neurons by inhibiting the inactivation of the MAPK pathway induced by HDAC2 .…”