Thymosin Beta 4 is overexpressed in human pancreatic cancer cells and stimulates proinflammatory cytokine secretion and JNK activation.

Zhang Y, Feurino LW, Zhai Q, Wang H, Fisher WE, Chen C, Yao Q, Li M

Cancer biology & therapy13 Dec 2007Cited by 44 (Europe PMC)

PMID18094619PMCIDPMC2930015DOI10.4161/cbt.7.3.5415PepBankPUB-18094619

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study5

4 results from studies that gave the peptide. No result from this study comes from people.

01LabIn vitro (cells)Mechanism
In Panc-1 pancreatic cancer cells, exogenous thymosin beta‑4 increased the secretion of IL-6.
In plain wordsIn cells, added thymosin beta‑4 made pancreatic cancer cells release more IL-6.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseIL-6 secretion in Panc-1 cells
Study
humann: not reported in source
Panc-1 human pancreatic cancer cells
Outcome group
Inflammation markers · Cancer
Studied dose
Dose not stated
Source sentences
Summary
Exogenous T beta 4 increased the secretion of proinflammatory cytokines IL-6, IL-8 and MCP-1 in Panc-1 cells.
1 context sentence(design, population, supporting numbers)
Summary · context
In the current study, we examined the expression of T beta 4 in pancreatic cancer cells, and determined the effect of exogenous T beta 4 on cytokine secretion, and signal transduction in human pancreatic cancer cells.
Report a problemFND-1809461902
02LabIn vitro (cells)Mechanism
In Panc-1 pancreatic cancer cells, exogenous thymosin beta‑4 increased the secretion of IL-8.
In plain wordsIn cells, added thymosin beta‑4 made pancreatic cancer cells release more IL-8.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseIL-8 secretion in Panc-1 cells
Study
humann: not reported in source
Panc-1 human pancreatic cancer cells
Outcome group
Inflammation markers · Cancer
Studied dose
Dose not stated
Source sentences
Summary
Exogenous T beta 4 increased the secretion of proinflammatory cytokines IL-6, IL-8 and MCP-1 in Panc-1 cells.
1 context sentence(design, population, supporting numbers)
Summary · context
In the current study, we examined the expression of T beta 4 in pancreatic cancer cells, and determined the effect of exogenous T beta 4 on cytokine secretion, and signal transduction in human pancreatic cancer cells.
Report a problemFND-1809461903
03LabIn vitro (cells)Mechanism
In Panc-1 pancreatic cancer cells, exogenous thymosin beta‑4 increased the secretion of MCP-1.
In plain wordsIn cells, added thymosin beta‑4 made pancreatic cancer cells release more MCP-1.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseMCP-1 secretion in Panc-1 cells
Study
humann: not reported in source
Panc-1 human pancreatic cancer cells
Outcome group
Inflammation markers · Cancer
Studied dose
Dose not stated
Source sentences
Summary
Exogenous T beta 4 increased the secretion of proinflammatory cytokines IL-6, IL-8 and MCP-1 in Panc-1 cells.
1 context sentence(design, population, supporting numbers)
Summary · context
In the current study, we examined the expression of T beta 4 in pancreatic cancer cells, and determined the effect of exogenous T beta 4 on cytokine secretion, and signal transduction in human pancreatic cancer cells.
Report a problemFND-1809461904
04LabIn vitro (cells)Mechanism
In human pancreatic cancer cells, thymosin beta‑4 activated Jun N-terminal Kinase signaling pathways.
In plain wordsIn cells, thymosin beta‑4 switched on the JNK signaling pathway in pancreatic cancer cells.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseJNK signaling activation
Study
humann: not reported in source
human pancreatic cancer cells
Outcome group
Receptor activity and mechanism · Cancer
Studied dose
Dose not stated
Source sentences
Summary
In addition, T beta 4 activated Jun N-terminal Kinase (JNK) signaling pathways in pancreatic cancer cells.
1 context sentence(design, population, supporting numbers)
Summary · context
In the current study, we examined the expression of T beta 4 in pancreatic cancer cells, and determined the effect of exogenous T beta 4 on cytokine secretion, and signal transduction in human pancreatic cancer cells.
Report a problemFND-1809461905

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

05LabEndogenous levelIn vitro (cells)Mechanism
Human pancreatic cancer cell lines expressed more thymosin beta‑4 mRNA than normal pancreatic ductal epithelium cells.
In plain wordsIn cells, pancreatic cancer cell lines made more of the body's own thymosin beta‑4 mRNA than normal duct cells.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseT beta 4 mRNA expression in pancreatic cancer cell lines
Study
humann: not reported in source
human pancreatic cancer cells
Comparator
Normal human pancreatic ductal epithelium (HPDE) cells
Outcome group
Tumor growth · Cancer
Source sentences
Summary
Pancreatic cancer cell lines expressed higher amount of T beta 4 mRNA than normal human pancreatic ductal epithelium (HPDE) cells.
1 context sentence(design, population, supporting numbers)
Summary · context
In the current study, we examined the expression of T beta 4 in pancreatic cancer cells, and determined the effect of exogenous T beta 4 on cytokine secretion, and signal transduction in human pancreatic cancer cells.
This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-1809461901

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
13 Oct 2026, 01:52 UTC
Study results updated
Version 1
12 Oct 2026, 18:17 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

Publication types

MeSH terms

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