Evidence map›Paper›PMID 32648126›Full record

ArticleChinese journal of integrative medicine2022

Kang-Ai Injection Inhibits Gastric Cancer Cells Proliferation through IL-6/STAT3 Pathway.

Chun-Lei Zheng, Ke-Zuo Hou, An-Qi Wang, Wan-Xia Fang, Shi-Tong Yu, Jin-E Liang, Hai-Yan Qi, Xiu-Juan Qu, Yun-Peng Liu, Xiao-Fang Che

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Article in Chinese journal of integrative medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

7 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

10 authors.

Chun-Lei ZhengDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, 110001, China.
Ke-Zuo HouDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, 110001, China.
An-Qi WangDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, 110001, China.
Wan-Xia FangDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, 110001, China.
Shi-Tong YuDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, 110001, China.
Jin-E LiangDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, 110001, China.
Hai-Yan QiDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, 110001, China.
Xiu-Juan QuDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, 110001, China.
Yun-Peng LiuDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, 110001, China.
Xiao-Fang CheDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, 110001, China. xfche@cmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo explore the mechanisms underlying the proliferative inhibition of Chinese herbal medicine Kang-Ai injection (KAI) in gastric cancer cells.

methodsGastric cancer cell lines MGC803 and BGC823 were treated by 0, 0.3%, 1%, 3% and 10% KAI for 24, 48 and 72 h, respectively. The cell proliferation was evaluated by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. The apoptosis and cell cycle were evaluated by flow cytometry. Interleukin (IL)-6 mRNA and protein expression levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immune sorbent assay (ELISA), respectively. The protein expression levels of cyclin A, cyclin E, cyclin B1, cyclin D1, p21, retinoblastoma (RB), protein kinase B (AKT), extracellular regulated protein kinases (ERK), signal transducer and activator of transcription (STAT) 1 and STAT3 were detected by Western blot.

resultsKAI inhibited the proliferation of MGC803 and BGC823 gastric cancer cells in dose- and time-dependent manner. After treated with KAI for 48 h, the proportion of G1 phase was increased, expression level of cyclin D1 and phosphorylation-RB were down-regulated, whereas the expression of p21 was up-regulated (all P<0.01). Furthermore, 48-h treatment with KAI decreased the phosphorylation level of STAT3, inhibited the mRNA and protein expressions of IL-6 (all P<0.01). IL-6 at dose of 10 ng/mL significantly attenuated the proliferative effect of both 3% and 10% KAI, and recovered KAI-inhibited STAT3 phosphorylation and cyclin D1 expression level (all P<0.01).

conclusionKAI exerted an anti-proliferative function by inhibiting IL-6/STAT3 signaling pathway followed by the induction of G

Indexed as

Interleukin-6Stomach NeoplasmsApoptosisCell Line, TumorCell ProliferationCyclin D1HumansRNA, MessengerSTAT3 Transcription FactorCyclin D1Interleukin-6RNA, MessengerSTAT3 protein, humanSTAT3 Transcription FactorChinese herbal medicineG1 arrestgastric cancerinterleukin-6Kang-Ai Injectionsignal transducer and activator of transcription 3

Identifiers

PMID32648126

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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.