We have previously shown that ethanol or chloroform extracts of the leaves ofImpatiens balsamina (LIB) have anti-tumor activity against the human hepatocellularcarcinoma cell line HepG2. The ethanol extracts were separated into five fractionsaccording to polarity. An MTT assay indicated that two of the fractions had anti-tumoractivity and that the petroleum ether fraction (PEF) was the most active. But the availablequantities of both the PEF and chloroform fractions (CHF) were limited, precluding furtherstudy. The chloroform extract (CHE) shared almost all the same spots with the PEF andCHF and was plentiful enough to carry out further separations. Thus, the CHE was furtherseparated into six sub-fractions (CHE1~6) by column chromatography. A MTT assayshowed that only the CHE2 fraction had a strong tumor inhibition ratio (IC50 = 6.47±0.05mg/L), which was superior to that of curcumin (IC50 = 13.95±0.11 mg/L). However, TLCrevealed that CHE2 was not pure and still contained two more components. After furtherseparation and purification, followed by TLC and MTT assay confirmation, the final activecomponent was isolated and identified as 2-methoxy-1,4-naphthoquinone by m.p., UV, MSand 13C- and 1H-NMR data. This is the first report demonstrating that2-methoxy-1,4-naphthoquinone has intensive in vitro anti-tumor activity against HepG2cells.
There are two types of abnormal hematopoiesis in solid tumor occurrence and treatment: pathological hematopoiesis, and myelosuppression induced by radiotherapy and chemotherapy. In this review we primarily focus on the abnormal pathological hematopoietic differentiation in cancer induced by tumor‐released granulocyte colony‐stimulating factor (G‐CSF) and granulocyte‐macrophage colony‐stimulating factor (GM‐CSF). As key factors in hematopoietic development, G‐CSF/GM‐CSF are well‐known facilitators of myelopoiesis and mobilization of hematopoietic stem cells (HSCs). In addition, these two cytokines can also promote or inhibit tumors, dependent on tumor type. In multiple cancer types, hematopoiesis is greatly enhanced and abnormal lineage differentiation is induced by these two cytokines. Here, dysregulated hematopoiesis induced by G‐CSF/GM‐CSF in solid tumors and its mechanism are summarized, and the prognostic value of G‐CSF/GM‐CSF‐associated dysregulated hematopoiesis for tumor metastasis is also briefly highlighted.
Metastasis remains the most deadly aspect of cancer and still evades direct treatment. Thus, there is a great need to develop new treatment regimens to suppress tumor cells that have escaped surgical removal or that may have already disseminated. We have found that tetrandrine (TET) exhibits anticolon cancer activity. Here, we investigate the inhibition effect of TET to breast cancer metastasis, angiogenesis and its molecular basis underlying TET’s anticancer activity. We compare TET with chemotherapy drug doxorubicin in 4T1 tumor bearing BALB/c mice model and find that TET exhibits an anticancer metastatic and antiangiogenic activities better than those of doxorubicin. The lung metastatic sites were decreased by TET, which is confirmed by bioluminescence imagingin vivo. On the other hand, laser doppler perfusion imaging (LDI) was used for measuring the blood flow of tumor in 4T1-tumor bearing mice. As a result, the local blood perfusion of tumor was markedly decreased by TET after 3 weeks. Mechanistically, TET treatment leads to a decrease in p-ERK level and an increase in NF-κB levels in HUVECs. TET also regulated metastatic and angiogenic related proteins, including vascular endothelial growth factor, hypoxia-inducible factor-1α, integrinβ5, endothelial cell specific molecule-1, and intercellular adhesion molecule-1in vivo.