Scientists uncover how cancer cells resist common chemotherapy

cancer drugs

Cancer is now the leading killer in wealthy countries and will soon be worldwide

Scientists from the University of New South Wales and the University of Technology Sydney have revealed how cancer cells circumvent a common cancer therapy.

The study, recently published in the Current Biology journal, showed that cancer cells can activate a force-generating rescue mechanism to stabilise an essential cell structure.

An essential cell structure responsible for cell division and resist the effects of chemotherapy.

Cancer cells use the mechanical force supplied by the cell cortex to overcome the impact of commonly used chemotherapy.

Peter Gunning, senior author of the study and Professor at the University of New South Wales, made this known.

“Now that we understand this exact pathway cancer cells use to avoid the toxic effects of the chemotherapy, it opens the door to improving cancer treatments.’’

During cell division or mitosis, microtubules inside cells help in the separation of genetic material.

Related News

Cancer cells divide more rapidly than normal ones, making them targets for chemotherapy drugs, which disrupt these microtubules.

Gunning said that high doses of this chemotherapy effectively induce cell death by causing chaos in chromosome separation, but at lower doses, cancer cells can start a rescue mechanism.

This mechanism involves the cancer cells recognising disrupted microtubules and activating a process to reconnect these fragments, ensuring cancer cell multiplication.

For their next step, researchers will focus on developing drugs that work in combination with current chemotherapy to overcome the cancer cell resistance mechanism.

Before testing on patients, these drugs would undergo refinement in animal models and preclinical studies.

“By attacking the force-generating machinery built by the cancer cells, we expect that we will be able to allow the cancer therapy to do its job much more effectively,’’ Gunning said. (Xinhua/NAN) (www.nannews.ng)

Load more