New study [1].
The taxane chemotherapy drugs get the name from the yew [genus Taxus]. We are perhaps more familiar with Docetaxel [Taxotere] but Paclitaxel [Taxol], from the Pacific yew, was the first.
"Paclitaxel (PTX) is a first-line chemotherapeutic drug for the treatment of prostate cancer.{?} However, most patients develop resistance and metastasis, and thus new therapeutic approaches are urgently required."
In a cell study - adding zinc [Zn] to Paclitaxel [PTX]:
"Zn and PTX increased proliferation inhibition in a dose- and time-dependent manner in prostate cancer cells, while Zn increased prostate cancer cell chemosensitivity to PTX."
"Our results demonstrated that Zn and PTX combined therapy inhibits EMT {epithelial-mesenchymal transition} by reducing the expression of TWIST1, which reduces the invasion and migration of prostate cancer cells."
"Therefore, Zn may be a potential adjuvant of PTX in treating prostate cancer and combined treatment may offer a promising therapeutic strategy for prostate cancer."
Worth a try if on one of the taxanes. I don't see a downside to the use of zinc.
-Patrick
ncbi.nlm.nih.gov/pubmed/307...
Prostate. 2019 Feb 3. doi: 10.1002/pros.23772. [Epub ahead of print]
Zinc promotes prostate cancer cell chemosensitivity to paclitaxel by inhibiting epithelial-mesenchymal transition and inducing apoptosis.
Xue YN1, Yu BB1, Liu YN1, Guo R1, Li JL1, Zhang LC1, Su J1, Sun LK1, Li Y1.
Author information
1
Department of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China.
Abstract
BACKGROUND:
Paclitaxel (PTX) is a first-line chemotherapeutic drug for the treatment of prostate cancer. However, most patients develop resistance and metastasis, and thus new therapeutic approaches are urgently required. Recent studies have identified widespread anti-tumor effects of zinc (Zn) in various tumor cell lines, especially prostate cancer cells. In this study, we examined the effects of Zn as an adjuvant to PTX in prostate cancer cells.
METHODS:
PC3 and DU145 cells were treated with different concentrations of Zn and/or PTX. MTT assay was used to detect cell viability. Real-time cell analysis (RTCA) and microscopy were used to observe morphological changes in cells. Western blotting was used to detect the expression of epithelial-mesenchymal transition (EMT)-related proteins. qPCR (reverse transcription-polymerase chain reaction) was used to examine changes in TWIST1 mRNA levels. Cell invasion and migration were detected by scratch and transwell assays. shRNA against TWIST1 was used to knockdown TWIST1. Colony formation assay was used to detect cell proliferation, while Annexin V and propidium iodide (PI) staining was used to detect cell apoptosis.
RESULTS:
Zn and PTX increased proliferation inhibition in a dose- and time-dependent manner in prostate cancer cells, while Zn increased prostate cancer cell chemosensitivity to PTX. Combined Zn and PTX inhibited prostate cancer cell invasion and migration by downregulating the expression of TWIST1. Furthermore, knockdown of TWIST1 increased the sensitivity of prostate cancer cells to PTX. In addition, Zn and PTX reduced cell proliferation and induced apoptosis in prostate cancer cells.
CONCLUSIONS:
Our results demonstrated that Zn and PTX combined therapy inhibits EMT by reducing the expression of TWIST1, which reduces the invasion and migration of prostate cancer cells. SiTWIST1 increased the sensitivity of prostate cancer cells to PTX. In addition, with prolonged treatment, Zn and PTX inhibited proliferation and led to prostate cancer cell apoptosis. Therefore, Zn may be a potential adjuvant of PTX in treating prostate cancer and combined treatment may offer a promising therapeutic strategy for prostate cancer.
© 2019 Wiley Periodicals, Inc.
KEYWORDS:
EMT; TWIST1; invasion; migration
PMID: 30714183 DOI: 10.1002/pros.23772