Evidence map›Paper›PMID 26846103›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

A novel derivative of tetrandrine (H1) induces endoplasmic reticulum stress-mediated apoptosis and prosurvival autophagy in human non-small cell lung cancer cells.

Yidan Lin, Yu Wang, Xianfang Liu, Jiamei Yan, Ling Su, Xiangguo Liu

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.5field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Endoplasmic reticulum stress in non-small cell lung cancer.American journal of cancer research · 2025
    Review
  4. Review
  5. Targeting the two-pore channel 2 in cancer progression and metastasis.Exploration of targeted anti-tumor therapy · 2022
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Role of Autophagy and Apoptosis in Non-Small-Cell Lung Cancer.International journal of molecular sciences · 2017
    Review
  12. Article
  13. Review
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

6 authors at 3 institutions in 1 country.

Yidan LinThe Thoracic Surgery Department of West China Hospital, West China Medical School of Sichuan University, Chengdu, China.
Yu WangThe Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Rm 103, South BLDG, 27 Shanda South Road, Jinan, 250100, China.
Xianfang LiuThe Department of Otolaryngology Head and Neck Surgery, Provincial Hospital Affiliated to Shandong University, Jinan, China.
Jiamei YanThe Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Rm 103, South BLDG, 27 Shanda South Road, Jinan, 250100, China.
Ling SuThe Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Rm 103, South BLDG, 27 Shanda South Road, Jinan, 250100, China.
Xiangguo LiuThe Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Rm 103, South BLDG, 27 Shanda South Road, Jinan, 250100, China. xgliu@sdu.edu.cn.
Shandong University · CNShandong Provincial Hospital · CNWest China Medical Center of Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

H1, a bromized derivative of tetrandrine, has been reported to induce apoptosis in human cancer cells. But, the underlying mechanism of apoptosis triggered by H1 is unclear. In the present study, we found that H1 triggered death receptor 5 (DR5)-dependent apoptosis in non-small cell lung cancer (NSCLC) cells. Further study showed that H1 activated ER stress through enforcing the expression of Bip/GRP78, IRE1α, p-eIF2α, and CHOP. Moreover, abrogating CHOP expression blocked DR5 upregulation and subsequent apoptosis, indicating that CHOP was essential for DR5-dependent apoptosis induced by H1. In addition, H1 greatly downregulated cellular FLICE-inhibitory protein (c-FLIP), and enhanced expression of c-FLIP protected cancer cells from apoptosis in spite of H1 therapy. Furthermore, we discovered that H1 induced autophagy in human NSCLC cells. Interestingly, the autophagy induced by H1 played a protective function in NSCLC cells and effectively weakened caspase-mediated apoptosis. In summary, these findings suggest that H1 induces DR5-dependent apoptosis in human NSCLC cells via stimulating ER stress signaling pathway, and pharmacologically inhibiting autophagy will be an efficient approach to synergize H1-caused apoptosis in lung cancer cells.

Indexed as

Antineoplastic AgentsApoptosisBenzylisoquinolinesBlotting, WesternCarcinoma, Non-Small-Cell LungCell Line, TumorEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressGene Knockdown TechniquesHumansLung NeoplasmsReceptors, TNF-Related Apoptosis-Inducing LigandAntineoplastic AgentsBenzylisoquinolinesEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanReceptors, TNF-Related Apoptosis-Inducing LigandtetrandrineTNFRSF10B protein, humanApoptosisAutophagyc-FLIPCHOPDR5ER stressTetrandrine

Identifiers

PMID26846103
OpenAlexW2301342528

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.