CSE1L/CAS, a microtubule-associated protein, inhibits taxol (paclitaxel)-induced apoptosis but enhances cancer cell apoptosis induced by various chemotherapeutic drugs

CSE1L/CAS, a microtubule-associated, cellular apoptosis susceptibility protein, is highly expressed in various cancers. Microtubules are the target of paclitaxel-induced apoptosis. We studied the effects of increased or reduced CAS expression on cancer cell apoptosis induced by chemotherapeutic drugs including paclitaxel. Our results showed that CAS overexpression enhanced apoptosis induced by doxorubicin, 5-fluorouracil, cisplatin, and tamoxifen, but inhibited paclitaxel-induced apoptosis of cancer cells. Reductions in CAS produced opposite results. CAS overexpression enhanced p53 accumulation induced by doxorubicin, 5-fluorouracil, cisplatin, tamoxifen, and etoposide. CAS was associated with alpha-tubulin and beta-tubulin and enhanced the association between alpha-tubulin and beta-tubulin. Paclitaxel can induce G2/M phase cell cycle arrest and microtubule aster formation during apoptosis induction, but CAS overexpression reduced paclitaxel-induced G2/M phase cell cycle arrest and microtubule aster formation. Our results indicate that CAS may play an important role in regulating the cytotoxicities of chemotherapeutic drugs used in cancer chemotherapy against cancer cells.

Medienart:

Artikel

Erscheinungsjahr:

2008

Erschienen:

2008

Enthalten in:

Zur Gesamtaufnahme - volume:41

Enthalten in:

BMB reports - 41(2008), 3 vom: 31. März, Seite 210-6

Sprache:

Englisch

Beteiligte Personen:

Liao, Ching-Fong [VerfasserIn]
Luo, Shue-Fen [VerfasserIn]
Shen, Tzu-Yun [VerfasserIn]
Lin, Chin-Huang [VerfasserIn]
Chien, Jung-Tsun [VerfasserIn]
Du, Shin-Yi [VerfasserIn]
Jiang, Ming-Chung [VerfasserIn]

Themen:

80168379AG
Antineoplastic Agents
Cellular Apoptosis Susceptibility Protein
Doxorubicin
Journal Article
Microtubule-Associated Proteins
P88XT4IS4D
Paclitaxel
Tubulin

Anmerkungen:

Date Completed 02.05.2008

Date Revised 08.06.2019

published: Print

Citation Status MEDLINE

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM17859685X