Evidence map›Paper›PMID 24531715›Full record

ArticleOncogene2015

Inhibition of ANKRD1 sensitizes human ovarian cancer cells to endoplasmic reticulum stress-induced apoptosis.

Y Lei, B R Henderson, C Emmanuel, P R Harnett, A deFazio

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.0field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 73 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Y Lei1] Department of Gynaecological Oncology, Westmead Hospital, Westmead, New South Wales, Australia [2] Westmead Institute for Cancer Research, University of Sydney at the Westmead Millennium Institute, Westmead, New South Wales, Australia.
B R HendersonWestmead Institute for Cancer Research, University of Sydney at the Westmead Millennium Institute, Westmead, New South Wales, Australia.
C Emmanuel1] Department of Gynaecological Oncology, Westmead Hospital, Westmead, New South Wales, Australia [2] Westmead Institute for Cancer Research, University of Sydney at the Westmead Millennium Institute, Westmead, New South Wales, Australia.
P R Harnett1] Westmead Institute for Cancer Research, University of Sydney at the Westmead Millennium Institute, Westmead, New South Wales, Australia [2] Crown Princess Mary Cancer Centre, Westmead Hospital, Westmead, New South Wales, Australia.
A deFazio1] Department of Gynaecological Oncology, Westmead Hospital, Westmead, New South Wales, Australia [2] Westmead Institute for Cancer Research, University of Sydney at the Westmead Millennium Institute, Westmead, New South Wales, Australia [3] Crown Princess Mary Cancer Centre, Westmead Hospital, Westmead, New South Wales, Australia.
University of Sydney · AUWestmead Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High expression of Ankyrin Repeat Domain 1 (ANKRD1) in ovarian carcinoma is associated with poor survival, and in ovarian cancer cell lines is associated with platinum resistance. Importantly, decreasing ANKRD1 expression using siRNA increases cisplatin sensitivity. In this study, we investigated possible mechanisms underlying the association of ANKRD1 with cisplatin response. We first demonstrated that cisplatin-induced apoptosis in ovarian cancer cell lines was associated with endoplasmic reticulum (ER) stress, evidenced by induction of Glucose-Regulated Protein 78 (GRP78), growth arrest- and DNA damage-inducible gene 153 (GADD153) and increased intracellular Ca(2+) release. The level of sensitivity to cisplatin-induced apoptosis was associated with ANKRD1 protein levels and poly (ADP-ribose) polymerase (PARP) cleavage. COLO 316 ovarian cancer cells, which express high ANKRD1 levels, were relatively resistant to cisplatin, and ER stress-induced apoptosis, whereas OAW42 and PEO14 cells, which express lower ANKRD1 levels, are more sensitive to ER stress-induced apoptosis. Furthermore, we show that overexpression of ANKRD1 attenuated cisplatin-induced cytotoxicity, and conversely siRNA knockdown of ANKRD1 sensitized ovarian cancer cells to cisplatin and ER stress-induced apoptosis associated with induction of GADD153, and downregulation of BCL2 and BCL-XL. Taken together, these results suggest that ANKRD1 has a significant role in the regulation of apoptosis in human ovarian cancer cells, and is a potential molecular target to enhance sensitivity of ovarian cancer to chemotherapy.

Indexed as

Apoptosisbcl-X ProteinCell Line, TumorCisplatinDrug Resistance, NeoplasmEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressFemaleHumansMuscle ProteinsNuclear ProteinsOvarian NeoplasmsPoly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-bcl-2Repressor ProteinsANKRD1 protein, humanBCL2L1 protein, humanbcl-X ProteinCisplatinEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanMuscle ProteinsNuclear ProteinsPoly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-bcl-2Repressor Proteins

Identifiers

PMID24531715
OpenAlexW2012086249

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.