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Table 2 Anticancer properties of XNT

From: Xanthorrhizol: a review of its pharmacological activities and anticancer properties

Types of cancer

Description

References

Breast cancer (MDA-MB-231, MCF-7, T47D, YMB-1, MDA-MB-453 and SK-BR-3 cells)

Induced mitochondrial-mediated apoptosis against MDA-MB-231 (↑ caspase-3, -9, cytochrome c and ↓ PARP-1) and MCF-7 cell apoptosis (↑ p53, ↓ Bcl-2 and PARP-1); acted as partial estrogen antagonist against T47D cell line

[12, 13, 18, 60, 63]

Colon cancer (HCT116 cells)

Induced cell cycle arrest (G0/G1, G2/M phase and increased sub-G1 peaks); mitochondrial pathway apoptosis (↑ caspase-8, -9 and-3), tBID and ↓ Bcl-XL protein, cleavage of PARP; ↑ NAG-1 may inactivate Akt pathway and subsequently suppressed GSK3β and mTOR

[65]

Cervical cancer (HeLa cells)

Induced p53 and Bax-dependent apoptosis, but not Bcl-2 and E6

[61]

Liver cancer (HepG2 cells)

Mitochondrial pathway apoptosis(↑ p53 ↓ Bcl-2 and Bcl-XL), but not Bax; caspase activation (caspase-3 and -9, not -7) involved tBid; cleavage of PARP and DFF45/ICAD proteins

[7, 14]

Skin cancer (HM3KO cells; TPA-induced tumor promotion in DMBA-initiated mouse skin)

Induced apoptosis in HM3KO cells; decreased tumor multiplicity and tumor incidence in DMBA-initiated mouse skin, suppressed ODC, COX-2 and iNOS expression through NF-kB (blocking IkBα degradation) and or Akt, inactivated ERK, p38, JNK and Akt

[26, 62]

Lung cancer (spontaneous mouse lung metastasis model)

Downregulation of MMP and COX-2 in MAPK/ERK pathway (decreased COX-2, MMP-9 and phosphorylated ERK); attenuated expression of JNK and p38; counteracted the effect of Raf-1

[41]

Tongue cancer (Tca8113 cells)

Induced cell cycle arrest in G0/G1 and S + G2/M phase; downregulated the protein expression of Bcl-2, but not Bax

[66]

Oral cancer (SCC-15 OSCC cells; DMBA-induced oral carcinogenesis in hamsters)

Caspase-independent apoptosis through ROS-mediated p38 MAPK and JNK activation in SCC-15 OSCC cells; inhibited the tumors number in buccal pouches in hamsters treated with DMBA

[67]

Esophageal cancer (TE-1 and TE-4 cells)

Reduced p-Akt and cyclin D1 expression; increased caspase-3 expression

[68]

Sarcoma 180 ascites

Lack of mechanism studies

[64]

Ovarian cancer (CaOV-3 cells)

Cytotoxic (lack of accessible information)

[62]

  1. PARP-1 poly-(ADP-ribose) polymerase-1, tBid truncation of bid, NAG-1 non-steroidal anti-inflammatory drug-activated gene-1, Akt protein kinase B, GSK3β glycogen synthase kinase-3beta, mTOR mammalian target of rapamycin, DFF45/ICAD DNA fragmentation factor 45/inhibitor of caspase-activated DNase, DMBA 7,12-dimethylbenz[a]anthracene, ERK extracellular signal-regulated kinase, MMP matrix metalloproteinase, Raf-1 Raf-1 proto-oncogene serine/threonine-protein kinase, OSCC oral squamous cell carcinoma, p-Akt phospho-protein kinase B