The Effect of Terpenoid Natural Chinese Medicine Molecular Compound on Lung Cancer Treatment

Table 3

The molecular mechanism of terpenoid natural Chinese medicine small molecules to promote tumor cell apoptosis in the treatment of lung cancer.

Terpenoid natural TCM small molecules	Experimental model	Dose/concentration	Mechanism of action	Ref.
Atractylodes macrocephala I (ATL-I)	A549 and HCC827 NSCLC cells	ATL-I (10, 20, and 40 μM) for 48 h	Upregulation of caspase-3, caspase-9, and Bax;	[39]
			Downregulation of Bcl-2 and Bcl-XL
Atractylodes macrocephala III (ATL-III)	A549 NSCLC cells	ATL-II I (1–100 μM) for 24 h	Increased lactate dehydrogenase release;	[40]
			Modulated cell cycle on A549 cells;
			Induced the release of cytochrome c;
			Upregulation of Bax expression
Costunolide	A549 NSCLC cells	Costunolide (0, 5, 10, 15, 25, or 30 μM) for 24 h	Upregulation of GRP78 and IRE1α and the activation of ASK1 and JNK;	[41]
			Induced ROS generation;
			Changed the antiapoptotic function of Bcl-2;
Costunolide	SK-MES-1 human lung squamous carcinoma cells	Costunolide (40 and 80 µM) for 24 h	Induced cell cycle arrest at G1/S phase;	[42]
			Upregulation in the expression of p53 and Bax;
			Downregulation in the expression of Bcl-2 and activation of caspase-3;
Pachymic acid (PA)	NCI-H23 and NCI-H460 lung cancer cells	PA (20, 40, or 80 µM) for 24 h	Induced cell cycle arrest at G2/M phase;	[43]
			Induced ROS generation;
			Activation of both c-Jun N-terminal kinase (JNK) and endoplasmic reticulum (ER) stress apoptotic pathways.
Pachymic acid (PA)	A549 NSCLC cells	PA (0, 3, 10, 30, 60, 100, and 200 µM) for 24 or 48 h	Inhibited anchorage-dependent and anchorage-independent A549 growth;	[44]
			Induced apoptosis of A549 cells;
			Decreased IL-1 beta-induced activation of cPLA (2) and COX-2;
			Suppressed IL-1 beta-induced activation of MAPKs;
			Inhibited IL-1 beta-stimulated nuclear factor kappa B of NF-kB;
Polyporenic acid C (PPAC)	A549 NSCLC cells	PPAC (0, 2, 6, 20, 60, or 200 µM) for 24, 48, or 72 h	Suppressed PI3-kinase/Akt signal pathway;	[45]
			Enhanced p53 activation.
Tubeimoside I (TBMS1)	NCI-H1299 and NCI-H1975 lung cancer cells	TBMS1 (0, 10, 20, and 30 µM) for 24 h	Induction of DRP1-mediated mitochondrial fragmentation;	[46]
			Inhibited V-ATPase and blocked late-stage autophagic flux via;
			Blocked the removal of dysfunctional mitochondria;
			Induced ROS generation.