How does camptothecin cause apoptosis?

How does camptothecin cause apoptosis?

Camptothecin caused apoptosis in SiHa cells by inducing mitochondrial membrane permeability changes that lead to the loss of mitochondrial membrane potential, decreased Bcl-2 levels, cytochrome c release, caspase-3 activation, formation of reactive oxygen species and depletion of GSH.

Does inhibition of apoptosis lead to cancer?

Apoptosis in Cancer The loss of apoptotic control allows cancer cells to survive longer and gives more time for the accumulation of mutations which can increase invasiveness during tumor progression, stimulate angiogenesis, deregulate cell proliferation and interfere with differentiation [2].

Which treatment triggers apoptosis?

Chemotherapy drugs and radiation work by forcing the cancer cells to undergo apoptosis, triggering death signals by causing DNA damage or cellular distress.

How does etoposide inhibit topoisomerase?

Etoposide kills cells by stabilizing a covalent enzyme-cleaved DNA complex (known as the cleavage complex) that is a transient intermediate in the catalytic cycle of topoisomerase II. If these breaks overwhelm the cell, they can initiate death pathways.

How does cisplatin cause apoptosis?

Cisplatin forms inter- and intrastrand crosslinked DNA adducts and its cytotoxicity is mediated by propagation of DNA damage recognition signals to downstream pathways involving ATR, p53, p73, and mitogen-activated protein kinases, ultimately resulting in apoptosis.

How does cancer inhibit apoptosis?

In some cases, cancer cells may escape apoptosis by increasing or decreasing expression of anti- or pro-apoptotic genes, respectively. Alternatively, they may inhibit apoptosis by stabilizing or de-stabilizing anti- or pro-apoptotic proteins, respectively.

What happens to apoptosis in an oncogenic condition?

Oncogene-induced apoptosis. Oncogenes such as E1A and c-myc induce apoptosis through p53-dependent and independent pathways, and both pathways may facilitate cytochrome c release from mitochondria. In any case, the Apaf-1/caspase-9 death effector complex appears important for oncogene-induced death.

Which of the following inhibits the action of topoisomerases?

Topoisomerase inhibitors in current use in the United States include irinotecan and topotecan, inhibitors of topoisomerase I, and etoposide and teniposide, inhibitors of topoisomerase II. All four agents are semisynthetic analogues of natural toxins that were initially identified in plants.

What happens if topoisomerase II is inhibited?

Inhibitors of topoisomerases I and II freeze these enzymes as protein-DNA complexes at various steps in their reaction pathways (31, 49). Topoisomerase-DNA-inhibitor complexes (cleavable complexes) are poisoned and are unable to execute a complete enzymatic cycle.

Is cisplatin-induced cell death always produced by apoptosis?

In summary, a growing body of evidence suggests that cisplatin-induced cell death does not always come from “classic”apoptosis. Depending on both cisplatin dose and cellular status, cisplatin may also induced cell death by a defective apoptotic program or even by necrosis.