Autophagy Regulated by Gain of Function Mutant p53 Enhances Proteasomal Inhibitor-Mediated Cell Death through Induction of ROS and ERK in Lung Cancer Cells.
Identifieur interne : 000067 ( PubMed/Curation ); précédent : 000066; suivant : 000068Autophagy Regulated by Gain of Function Mutant p53 Enhances Proteasomal Inhibitor-Mediated Cell Death through Induction of ROS and ERK in Lung Cancer Cells.
Auteurs : Heena Saini [Inde] ; Ifrah Hakeem [Inde] ; Sudeshna Mukherjee [Inde] ; Shibasish Chowdhury [Inde] ; Rajdeep Chowdhury [Inde]Source :
- Journal of oncology [ 1687-8450 ] ; 2019.
Abstract
Mutations in p53, especially gain of function (GOF) mutations, are highly frequent in lung cancers and are known to facilitate tumor aggressiveness. Yet, the links between mutant GOF-p53 and lung cancers are not well established. In the present study, we set to examine how we can better sensitize resistant GOF-p53 lung cancer cells through modulation of cellular protein degradation machineries, proteasome and autophagy. H1299 p53 null lung cancer cells were stably transfected with R273H mutant GOF-p53 or wild-type (wt) p53 or empty vectors. The presence of R273H-P53 conferred the cancer cells with drug resistance not only against the widely used chemotherapeutic agents like cisplatin (CDDP) or 5-flurouracil (5-FU) but also against potent alternative modes of therapy like proteasomal inhibition. Therefore, there is an urgent need for new strategies that can overcome GOF-p53 induced drug resistance and prolong patient survival following failure of standard therapies. We observed that the proteasomal inhibitor, peptide aldehyde N-acetyl-leu-leu-norleucinal (commonly termed as ALLN), caused an activation of cellular homeostatic machinery, autophagy in R273H-P53 cells. Interestingly, inhibition of autophagy by chloroquine (CQ) alone or in combination with ALLN failed to induce enhanced cell death in the R273H-P53 cells; however, in contrast, an activation of autophagy by serum starvation or rapamycin increased sensitivity of cells to ALLN-induced cytotoxicity. An activated autophagy was associated with increased ROS and ERK signaling and an inhibition of either ROS or ERK signaling resulted in reduced cytotoxicity. Furthermore, inhibition of GOF-p53 was found to enhance autophagy resulting in increased cell death. Our findings provide novel insights pertaining to mechanisms by which a GOF-p53 harboring lung cancer cell is better sensitized, which can lead to the development of advanced therapy against resistant lung cancer cells.
DOI: 10.1155/2019/6164807
PubMed: 30723502
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wicri:level="1"><nlm:affiliation>Department of Biological Sciences, Pilani Campus, BITS, Pilani, Rajasthan 333031, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Department of Biological Sciences, Pilani Campus, BITS, Pilani, Rajasthan 333031</wicri:regionArea></affiliation></author><author><name sortKey="Mukherjee, Sudeshna" sort="Mukherjee, Sudeshna" uniqKey="Mukherjee S" first="Sudeshna" last="Mukherjee">Sudeshna Mukherjee</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biological Sciences, Pilani Campus, BITS, Pilani, Rajasthan 333031, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Department of Biological Sciences, Pilani Campus, BITS, Pilani, Rajasthan 333031</wicri:regionArea></affiliation></author><author><name sortKey="Chowdhury, Shibasish" sort="Chowdhury, Shibasish" uniqKey="Chowdhury S" first="Shibasish" last="Chowdhury">Shibasish Chowdhury</name><affiliation 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type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mutations in p53, especially gain of function (GOF) mutations, are highly frequent in lung cancers and are known to facilitate tumor aggressiveness. Yet, the links between mutant GOF-p53 and lung cancers are not well established. In the present study, we set to examine how we can better sensitize resistant GOF-p53 lung cancer cells through modulation of cellular protein degradation machineries, proteasome and autophagy. H1299 p53 null lung cancer cells were stably transfected with R273H mutant GOF-p53 or wild-type (wt) p53 or empty vectors. The presence of R273H-P53 conferred the cancer cells with drug resistance not only against the widely used chemotherapeutic agents like cisplatin (CDDP) or 5-flurouracil (5-FU) but also against potent alternative modes of therapy like proteasomal inhibition. Therefore, there is an urgent need for new strategies that can overcome GOF-p53 induced drug resistance and prolong patient survival following failure of standard therapies. We observed that the proteasomal inhibitor, peptide aldehyde N-acetyl-leu-leu-norleucinal (commonly termed as ALLN), caused an activation of cellular homeostatic machinery, autophagy in R273H-P53 cells. Interestingly, inhibition of autophagy by chloroquine (CQ) alone or in combination with ALLN failed to induce enhanced cell death in the R273H-P53 cells; however, in contrast, an activation of autophagy by serum starvation or rapamycin increased sensitivity of cells to ALLN-induced cytotoxicity. An activated autophagy was associated with increased ROS and ERK signaling and an inhibition of either ROS or ERK signaling resulted in reduced cytotoxicity. Furthermore, inhibition of GOF-p53 was found to enhance autophagy resulting in increased cell death. Our findings provide novel insights pertaining to mechanisms by which a GOF-p53 harboring lung cancer cell is better sensitized, which can lead to the development of advanced therapy against resistant lung cancer cells.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">30723502</PMID><DateRevised><Year>2020</Year><Month>02</Month><Day>25</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1687-8450</ISSN><JournalIssue CitedMedium="Print"><Volume>2019</Volume><PubDate><Year>2019</Year></PubDate></JournalIssue><Title>Journal of oncology</Title><ISOAbbreviation>J Oncol</ISOAbbreviation></Journal><ArticleTitle>Autophagy Regulated by Gain of Function Mutant p53 Enhances Proteasomal Inhibitor-Mediated Cell Death through Induction of ROS and ERK in Lung Cancer Cells.</ArticleTitle><Pagination><MedlinePgn>6164807</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1155/2019/6164807</ELocationID><Abstract><AbstractText>Mutations in p53, especially gain of function (GOF) mutations, are highly frequent in lung cancers and are known to facilitate tumor aggressiveness. Yet, the links between mutant GOF-p53 and lung cancers are not well established. In the present study, we set to examine how we can better sensitize resistant GOF-p53 lung cancer cells through modulation of cellular protein degradation machineries, proteasome and autophagy. H1299 p53 null lung cancer cells were stably transfected with R273H mutant GOF-p53 or wild-type (wt) p53 or empty vectors. The presence of R273H-P53 conferred the cancer cells with drug resistance not only against the widely used chemotherapeutic agents like cisplatin (CDDP) or 5-flurouracil (5-FU) but also against potent alternative modes of therapy like proteasomal inhibition. Therefore, there is an urgent need for new strategies that can overcome GOF-p53 induced drug resistance and prolong patient survival following failure of standard therapies. We observed that the proteasomal inhibitor, peptide aldehyde N-acetyl-leu-leu-norleucinal (commonly termed as ALLN), caused an activation of cellular homeostatic machinery, autophagy in R273H-P53 cells. Interestingly, inhibition of autophagy by chloroquine (CQ) alone or in combination with ALLN failed to induce enhanced cell death in the R273H-P53 cells; however, in contrast, an activation of autophagy by serum starvation or rapamycin increased sensitivity of cells to ALLN-induced cytotoxicity. An activated autophagy was associated with increased ROS and ERK signaling and an inhibition of either ROS or ERK signaling resulted in reduced cytotoxicity. Furthermore, inhibition of GOF-p53 was found to enhance autophagy resulting in increased cell death. Our findings provide novel insights pertaining to mechanisms by which a GOF-p53 harboring lung cancer cell is better sensitized, which can lead to the development of advanced therapy against resistant lung cancer cells.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Saini</LastName><ForeName>Heena</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, Pilani Campus, BITS, Pilani, Rajasthan 333031, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hakeem</LastName><ForeName>Ifrah</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, Pilani Campus, BITS, Pilani, Rajasthan 333031, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mukherjee</LastName><ForeName>Sudeshna</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0002-7731-1873</Identifier><AffiliationInfo><Affiliation>Department of Biological Sciences, Pilani Campus, BITS, Pilani, Rajasthan 333031, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chowdhury</LastName><ForeName>Shibasish</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0001-9290-3802</Identifier><AffiliationInfo><Affiliation>Department of Biological Sciences, Pilani Campus, BITS, Pilani, Rajasthan 333031, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chowdhury</LastName><ForeName>Rajdeep</ForeName><Initials>R</Initials><Identifier Source="ORCID">0000-0001-7652-4984</Identifier><AffiliationInfo><Affiliation>Department of Biological Sciences, Pilani Campus, BITS, Pilani, Rajasthan 333031, India.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>01</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>Egypt</Country><MedlineTA>J Oncol</MedlineTA><NlmUniqueID>101496537</NlmUniqueID><ISSNLinking>1687-8450</ISSNLinking></MedlineJournalInfo></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>07</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2018</Year><Month>10</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2018</Year><Month>12</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>2</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>2</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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