How Cancer Grows? Normal Cell Cycle Diagram & Cancerous Cell Cycle
Cancer ranks among the foremost causes of death worldwide, characterised by the abnormal and uncontrolled proliferation of cells triggered by genetic and epigenetic alterations. According to global health statistics, nearly 10 million deaths in 2020 were attributed to various forms of cancer, including breast, lung, colorectal, prostate, skin, and stomach cancers. [1] Cancer cells differ from normal cells primarily in their rapid division and ability to evade natural cell death mechanisms. As these malignant cells accumulate, they form tumours, which demand a continuous supply of nutrients and oxygen. In order to maintain their rapid expansion, cancer cells trigger the development of new blood vessels, a mechanism known as angiogenesis. This not only supports tumour expansion but also facilitates metastasis, allowing cancer to spread to other parts of the body. Current therapeutic research is exploring angiogenesis inhibitors as a strategy to restrict tumour progression and improve patient outcomes. [2]
MECHANISM OF ACTION
The therapeutic effectiveness of vinca alkaloids in cancer treatment is primarily attributed to their interaction with tubulin, a key structural protein in microtubules. These alkaloids disrupt the microtubule network by binding to specific sites on β-tubulin, particularly within the region referred to as the "vinca domain."[3] This binding interferes with the dynamic equilibrium of microtubule assembly and disassembly, essential for mitotic spindle formation during cell division. [4] As a result, the treated cells experience arrest at the metaphase stage of mitosis, ultimately leading to programmed cell death or apoptosis. Interestingly, even at low concentrations, vinca alkaloids can significantly alter microtubule dynamics by reducing both their growth and shrinkage rates. This stabilises the microtubules in a dysfunctional state, halting cell proliferation. [5] Beyond their role in mitosis, vinca alkaloids also impact non-dividing cells by affecting other microtubule-associated cellular processes. This includes intracellular transport and cell signalling pathways. Moreover, these compounds have shown potential in inhibiting tumour angiogenesis, thereby limiting the blood supply essential for tumour survival and growth. Such effects further enhance their anti-cancer potential, especially when used in combination with other chemotherapeutic agents or anti-angiogenic therapies. [6]
Priti Bhure*
Rajashri Wagh
Trupti Bankar
Shital Karhale
Vikram Saruk
10.5281/zenodo.17239644