Colorectal cancer (CRC) is one of the most commonly diagnosed cancer types worldwide. Despite significant advances in prevention and diagnosis, CRC is still one of the leading causes of cancer-related mortality globally. RAB27A, the member of RAB27 family of small GTPases, is the critical protein for intracellular secretion and has been reported to promote tumor progression. However, it is controversial for the role of RAB27A in CRC progression, so we explored the exact function of RAB27A in CRC development in this study. Based on the stable colon cancer cell lines of RAB27A knockdown and ectopic expression, we found that RAB27A knockdown inhibited proliferation and clone formation of SW480 colon cancer cells, whereas ectopic expression of RAB27A in RKO colon cancer cells facilitated cell proliferation and clone formation, indicating that RAB27A is critical for colon cancer cell growth. In addition, our data demonstrated that the migration and invasion of colon cancer cells were suppressed by RAB27A knockdown, but promoted by RAB27A ectopic expression. Therefore, RAB27A is identified as an onco-protein in mediating CRC development, which may be a valuable prognostic indicator and potential therapeutic target for CRC.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9653419PMC
http://dx.doi.org/10.1038/s41598-022-23696-7DOI Listing

Publication Analysis

Top Keywords

colon cancer
20
cancer cells
16
rab27a knockdown
12
ectopic expression
12
expression rab27a
12
rab27a
11
cancer
8
colorectal cancer
8
rab27a crc
8
crc development
8

Similar Publications

Background: Few studies have explored the genetic changes and clinicopathological features of stage II/III gastric cancer (GC) patients with no tumor recurrence, early recurrence, or late recurrence after curative surgery.

Methods: In this study, 376 patients who underwent curative surgery for stage II/III GC were analyzed. The clinical and genetic features of patients with no recurrence, early recurrence (<2 years), and late recurrence (≥2 years) were compared.

View Article and Find Full Text PDF

NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 4-like 2 (NDUFA4L2) protein is located in the mitochondria and can regulate cell proliferation. Some studies have shown that the high NDUFA4L2 expression is linked with poor prognosis and cancer progression in various patients with cancers. However, the correlation between NDUFA4L2 and pan-cancer is unknown.

View Article and Find Full Text PDF

Background: Lymphadenectomy for rectal cancer is clearly defined by total mesorectal excision (TME). The analogous surgical strategy for the colon, the complete mesocolic excision (CME), follows the same principles of dissection in embryologically predefined planes.

Method: This narrative review initially identified key issues related to lymphadenectomy of rectal and colon cancer.

View Article and Find Full Text PDF

LZZAY01 accelerated autophagy and apoptosis in colon cancer cells and improved gut microbiota in CAC mice.

Microbiol Spectr

January 2025

Laboratory of Microbiology and Immunology, School of Basic Medical Science, Inner Mongolia Medical University, Hohhot, China.

Colorectal cancer (CRC) is one of the malignant tumors globally, with high morbidity and mortality rates. The mainstay treatment of CRC includes surgery, radiotherapy, and chemotherapy. However, these treatments are associated with a high recurrence rate, poor prognosis, and highly toxic side effects.

View Article and Find Full Text PDF

Angiogenesis is an intricate pathway that involves the formation of new blood capillaries from old, functioning ones. Improper angiogenesis is a feature of numerous maladies, including malignancy and autoimmune disorders. Indole-related derivatives are believed to interfere with the mitotic spindle, inhibiting the multiplication, and invasion of cancerous human cells.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!