The prostate gland is a tiny walnut like shape gland in men’s pelvic. It’s right adjacent to the bladder and can the doctors can check it with a digital rectal exam. Prostate cancer is a type of cancer that starts in the prostate gland and spreads throughout the body. By breaking out from a prostate tumour, prostate cancer cells can spread and migrate to other parts of the body via blood arteries or lymph nodes.
Some of the current prostate cancer treatments are radiation therapy or combination therapy, non-steroidal antiandrogens, steroidal administration, chemotherapy, and surgery. Although these various treatment options can help to slow the progression of prostate cancer; they also link to other disorders that impact sexual and urinary function. As a result, prostate cancer research focuses on developing enhanced treatment options; to avoid some of the difficulties that can arise. Androgen ablation therapy is a treatment for prostate cancer that inhibits the action of the androgen receptor (AR).
The ability of prostate cancer to respond to testosterone stimulation is essentially androgen-sensitive or androgen-insensitive. Androgens stimulate prostate epithelial development and survival by binding to and activating the androgen receptor (AR). The AR–androgen complex works as a nuclear transcription factor for the activation of genes; that promote the synthesis of prostate-specific antigen (PSA) and proteins involved in cell proliferation; after intranuclear compartmentalization from the cytoplasm and DNA binding. Early-stage prostate cancer relies largely on AR activation for survival; although androgen-independent tumours typically mark the recurrence due to adaptations to low androgen levels. Surrogate AR pathways arise with an enhancing signalling due to an increase in the receptor sensitivity; or when one does not require androgen binding at all. Prostate tumours that lack AR function skip androgen receptor signalling and activate ot+7her survival pathways, allowing them to spread.
Curcumin has been shown in multiple studies to induce apoptosis and inhibit prostate cancer proliferation; in both in vitro and in vivo testing by interfering with several cellular pathways; including nuclear factor kappa B, epidermal growth factor, and mitogen-activated protein kinase. Curcumin compounds with increased solubility and anticancer effectiveness have been developed due to their low bioavailability, low cancer-killing potency, and numerous biological effects. Because curcumin has a low bioavailability, the amounts required to exert anticancer action in patients’ blood plasma are difficult to achieve. As a result, experts have expend much effort in the synthesis of curcumin derivatives; with effective anticancer activities and lower concentration values than curcumin.
When compared to curcumin, the anticancer activity of the curcumin derivative was increased; but the therapeutic efficacy and method of action are yet unknown; which is important to address because curcumin targets numerous signalling pathways. Dimethyl curcumin is another curcumin derivative that increases androgen receptor (AR) degradation and has been in use to treat prostate cancer. According to the research on curcumin derivatives’ structure-activity relationships; the presence of a beta-diketone and a coplanar hydrogen donor group hybrid is significant for antiandrogenic activity in the treatment of prostate cancer.
Curcumin demonstrates to reduce the viability, proliferation, survival, migration/invasion, and adhesion of several human prostate cancer cells in vitro experiments. Curcumin inhibited both androgen-sensitive and androgen-insensitive prostate cancer cells; by targeting a number of signalling pathways involved in cellular function regulation. Curcumin’s antiproliferative, antisurvival, and anti-migratory effects in prostate cancer cells could be due to signal transduction pathway inhibition; decreased nuclear factor kappa B activation; and increased proapoptotic caspase and PARP(protein enzyme) cleavage, and inhibition of antiapoptotic Bcl-2 family proteins. Curcumin could also induce cell-cycle arrest and boost autophagy in prostate cancer cell lines.
On the other hand, evidence suggesting curcumin to decrease the growth/volume, formation, development, proliferation, and angiogenesis of prostate cancer tumours while increasing apoptosis in vivo tests. Researchers xenografted both androgen-sensitive and androgen-insensitive prostate cancer cells into mice, resulting in these outcomes. Curcumin may inhibit prostate tumour growth and progression by inhibiting protein kinase B expression and activation, decreasing nuclear factor kappa B activation, inhibiting the anti-apoptotic proteins Bcl-2 and Bcl-xL, increasing expression of the pro-apoptotic proteins Bax and Bak, and increasing PARP (protein enzyme) and caspase expression. The results of the in vivo experiments are consistent with those of the in vitro trials.
Curcumin is a promising option for the development of novel anticancer pharmacological drugs due to its low toxicity and downregulation of cell growth in combination with increased activity of programmed cell death both in vitro and in vivo. Future in vitro studies should concentrate on using cell culture parameters like varied oxygen levels and glucose concentrations to acquire data that better represents the tumour microenvironment seen in vivo. Furthermore, we need more research using normal prostate epithelium to see if curcumin can distinguish between malignant and healthy tissue when interfering with signalling pathways.
Researchers will require several clinical prostate cancer cell lines to correctly establish curcumin dosage and to study if curcumin has powerful effects against prostate cancer in vivo. Finally, we need clinical trials to determine whether curcumin is useful against human prostate cancer.