HDAC10 Gene Editing    

At first, the biological role of histone deacetylases (HDACs) was known to be limited to their effect on histones; however, over the past few years, many groups have shown that their function includes more complex regulatory roles. These functions seem to be tissue specific, depending on the cellular compartment and stage of cellular differentiation. Among the HDACs, HDAC10 is a novel class IIb histone. HDAC10 is widely expressed and is found in both the cytoplasm and the nucleus; in addition, it derives as two spliced transcription variants that encode residues 658 and 669. In recent years, several reports have suggested that the expression of HDAC10 plays an important role in tumor suppression. For example, overexpression of HDAC10 in cervical cancer cells robustly inhibits metastasis by inhibiting the expression of matrix metalloproteinase (MMP) 2 and 9. Other studies have also shown that decreased expression of HDAC10 in lung cancer and gastric cancer predicts adverse and poor prognosis for the patients.

HDAC10 Promotes Lung Cancer Proliferation

HDAC10 is highly expressed in lung cancer tissues. It mainly exists in the cytoplasm of lung cancer cells but resides in the nucleus of adjacent normal cells. HDAC10 exists in the cytoplasm in multiple lung cancer cell lines, including the A549, H358 and H460 cell lines, but mainly exists in the nucleus of normal lung epithelial 16HBE cells. HDAC10 knockdown decreases AKT phosphorylation and that overexpression of AKT rescues the cell cycle arrest and apoptosis induced by HDAC10 knockdown, suggesting that AKT is related to the function of HDAC10 in lung cancer. A co-immunoprecipitation assay showed that HDAC10 interacts with AKT and that inhibition of HDAC10 activity decreases its interaction with and phosphorylation of AKT. Moreover, researchers confirmed that HDAC10 promoted lung cancer proliferation in a mouse model. These studies suggest that HDAC10 expression and localization may be valuable prognostic markers or potential therapeutic targets for lung cancer patients.

HDAC10 as A Therapeutic Target in Ovarian Cancer

The standard front-line adjuvant therapy for ovarian cancer includes platinum-based chemotherapy. The initial response is often promising, with 80% of patients responding to platinum. Unfortunately, most patients relapse and die of chemotherapy resistant disease. As long as ovarian tumors are sensitive to cisplatin, progression of the cancer will be arrested; therefore, any mechanism for maintaining cisplatin sensitivity of tumors is desirable. Some studies have found that serous ovarian cancers more commonly have HDAC10 deletions than the general population and in ovarian cancers homozygous deletion of HDAC10 correlated with tumor sensitivity to cisplatin. HDAC inhibitors potentiated the cytotoxicity of cisplatin in primary ovarian cancer cell lines derived from tumor ascites and potentiated the inhibition by cisplatin of DNA repair by homologous recombination. These results suggested that HDAC inhibition of HDR could enhance the first line platinum therapy and improve survival in patients with ovarian cancer. Several clinical trials are already underway of HDAC inhibitors (including SAHA) combined with platinum-based chemotherapy in ovarian cancer. Preclinical studies confirmed the finding of platinum sensitization in ovarian cancer cells using other ovarian cell lines when treated with SAHA. In conclusion, HDAC10 inhibition enhances the platinum sensitization of ovarian carcinoma cells. Interestingly, even in the ovarian cell line with BRCA1 deleted, HDAC10 stimulated DSB repair.

HDAC10 Gene Editing Services

CRISPR/Cas9 Platform^CB at Creative Biogene is dedicated to offering comprehensive CRISPR/Cas9 gene editing services and products for academic research, biotech research and pharmaceutical drug discovery. With deep gene editing knowledge and extensive experience in experimental operation and data processing, we help you effectively control HDAC10 genes knockout/knockin/point mutation in cells or animals via CRISPR/Cas9 technology.

Service	Details	Alternative cell lines or animal species
HDAC10 Gene Editing Cell Line Generation	gRNA design and synthesis Transfect the cell pnes you’re interested Select the high expression cells and sort monoclonal cell Vapdate the knockout/knockin/point mutation of HDAC10 by PCR and sequencing Provide cryogenically preserved vials of stable cells and final reports	HEK239T, Hela, HepG2, U87, Ba/F3, CHO, MDA-MB-453, MDA-MB-231NIH3T3, T47D, Neuro2a, MCF7, RKO, K562, RAW264.7, etc.
HDAC10 Gene Editing Animal Model Generation	HDAC10 gene conventional knockout animals HDAC10 gene conditional knockout animals HDAC10 point mutation animals HDAC10 knockin animals	Mouse, rat, rabbit, zebrafish, C. elegans, etc.

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