Evidence map›Paper›PMID 35342361›Full record

ArticleInternational journal of biological sciences2022

Icariside II enhances cisplatin-induced apoptosis by promoting endoplasmic reticulum stress signalling in non-small cell lung cancer cells.

Zhao Tang, Wenjing Du, Fei Xu, Xianjun Sun, Wenjing Chen, Jie Cui, Weifeng Tang, Fangyong Yang, Fangzhou Teng, Jinpei Lin and 2 more

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. A comprehensive narrative review ofJournal of pharmaceutical analysis · 2026
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  3. Article
  4. Article
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  12. Endoplasmic reticulum stress in non-small cell lung cancer.American journal of cancer research · 2025
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
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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

12 authors at 3 institutions in 1 country.

Zhao TangDepartment of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Wenjing DuDepartment of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Fei XuDepartment of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Xianjun SunDepartment of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Wenjing ChenDepartment of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Jie CuiDepartment of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Weifeng TangDepartment of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Fangyong YangDepartment of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Fangzhou TengDepartment of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Jinpei LinDepartment of Integrated TCM & Western Medicine Department, Fujian Cancer Hospital & Fujian Medical University Cancer Hospital, Fuzhou, China.
Baojun LiuDepartment of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Jingcheng DongDepartment of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Huashan Hospital · CNFudan University · CNFujian Provincial Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although cisplatin is the most effective first-line drug in the management of advanced non-small cell lung cancer (NSCLC), drug resistance remains a major clinical challenge. There is increasing evidence that icariside II (IS) exhibits antitumour activity in a variety of cancers. In the current study, we investigated the anticancer effects of icariside II combined with cisplatin and elucidated the underlying mechanism in NSCLC. Here, we showed that cotreatment with IS and cisplatin inhibited cell proliferation and induced cellular apoptosis. Using mRNA sequencing (mRNA-seq), we identified differentially expressed genes (DEGs) in which there was an enrichment in PERK-mediated unfolded protein response (UPR) signalling. The western blot results revealed that IS activated endoplasmic reticulum (ER) stress, including three branches of UPR signalling, PERK, IRE1 and ATF6, and the downstream PERK-eIF2α-ATF4-CHOP pathway, thus potentiating the apoptosis induced by cisplatin. In addition, the combination of IS with cisplatin significantly reduced xenograft tumour growth in C57BL/6 and BALB/c nude mice

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsAnimalsApoptosisCell Line, TumorCisplatineIF-2 KinaseEndoplasmic Reticulum StressFlavonoidsHumansMiceMice, Inbred C57BLMice, NudeRNA, Messengerbaohuoside ICisplatineIF-2 KinaseFlavonoidsRNA, Messengerapoptosiscisplatinendoplasmic reticulum stressicariside IIlung cancerunfolded protein response

Identifiers

PMID35342361
PMCPMC8935239
OpenAlexW4226357927

What OpenQuestion holds

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LicenceCC BY
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.